CHD represents a clinical phenotype in which inflammatory mediators are involved, including environmental risk factors and genetic susceptibility. Management of lipid parameters is very important in the clinical management of the disease. Therefore, the identification of gene regions known to have genetic effects on lipid profiles and their functional variants is very important in order to reduce the comorbidities of the disease by establishing early treatment protocols. In recent years, in studies conducted to determine predictors in CHD pathogenesis, a new candidate locus has been associated with CHD due to its effect on 1p13.3 lipid parameters (11–13, 17). Although the complex scenario of sortilin's role in lipid metabolism has not been explained yet, according to the information we have obtained from experimental and functional studies, hepatic sortilin can act as a receptor for LDL-C, independent of its LDLR (18). Interestingly, the SORT1 gene has been shown to bind the LDL receptor-associated protein (RAP) in vitro, thus providing a potential functional link to lipoprotein metabolism (19). In their experimental study using Sort1 (- / -) mice, Patel et al. Reported that Sort1 deficiency significantly reduced atherosclerosis by reducing LDL uptake of macrophages without creating any change in LDL-C levels (12). Another important task of Sortilin is its effect on inflammatory cytokines whose contribution to the atherosclerotic process is well known. It has been reported that sortilin deficiency alleviates inflammation by affecting the secretion of interleukin-6 (20). Due to its lipid regulation and inflammatory effects, sortie appears to be a very powerful mediator in the atherogenic process and a strong predictor of CHD risk. The SORT1 rs599839 polymorphism has been frequently associated with lipid levels and has been reported to be protective against CHD, usually due to the decrease in LDL-C levels (21, 22). However, there is no study conducted in the Turkish population related to this variant. Our study is the first Turkish study to examine the relationship between the SORT1 rs599839 polymorphism and lipid profile and CHD. According to our study data, the SORT1 rs599839 polymorphism does not appear to be effective in the pathogenesis of CAD. Our study data is Zhou. and Sánchez Muñoz-Torrero (21, 23, 24). Zou et al. reported that rs599839 and rs464218 variants were not effective in CHD pathogenesis in their case-control study in patients with CHD and ischemic stroke. Similarly, the data of a study conducted in the Spanish familial hypercholesterolemia cohort have recently published their studies reporting that there is no relationship between rs599839 alleles and CHD. Inconsistent with the data of these studies, the LURIC study data also reported that the AG and GG genotypes were more represented in the control groups compared to the CHD group, and this difference was statistically significant (p = 0.004). Studies conducted in the Chinese Han population also reported that the minor G allele was higher in the control group compared to the premature coronary heart disease group (p = 0.004) (25). Inconsistent data among the results of the studies may be related to sample size, ethnic differences, different genotypic frequencies, gene-environment interactions. The SORT1 rs599839 polymorphism; It can increase HDL-C level while decreasing the level of Total-K and LDL-C (21, 26, 27). Functional studies have demonstrated that the 1p13.3 rs599839 variants regulate cholesterol metabolism through regulation of sortilin expression and LDL-C uptake in hepatocytes and affect the diameter of circulating LDL-C particles of nature (28, 29). While the presence of the G allele did not affect triglyceride levels in accordance with the literature, a statistically significant decrease was observed in LDL-C and Total-C levels (30). This decline is consistent with data from studies in the Arab population (27), Austrians (31), Indians (32), Japanese (33), Chinese (34), Pakistanis (35), and Mexicans (36). We think that this decrease in LDL-C levels is due to the increase in intracellular uptake of LDL caused by the increased SORT1 expression in the presence of minor G allele, which is consistent with the previous study data (28). The 46% increase in Total-C levels caused by the reduction of SORT1 expression by siRNA and the more than the two-fold increase observed in LDL-C levels also support this idea (10). However, our study data are inconsistent with the study data reporting high Total-C levels observed in the Dutch population (37). An additional finding in this study is the high HDL-C levels we observed in the presence of the G allele. While this finding is consistent with the study of Zhou et al., It is inconsistent with the study data of Gigante et al. (30, 38). The differences in these results can be explained by the high linkage imbalance in allele frequency and sample size between different ethnic populations, with additional variants in genes involved in the lipid metabolism pathway of this SNP (27). We found that other cardiovascular risk factors HDL-C, Total-C, hypertension, diabetes (p < 0.001) and hyperlipidemia examined in our study had significant effects on the development of CHD (39–47). Our study confirms the importance of hypertension and hyperlipidemia in the pathogenesis of male CHD disease. Based on our findings from our study, we would like to report that the rs599839 variant does not contribute directly to the pathogenesis of CHD in Turks. However, considering the positive effect of this variant on lipid profiles, we think that the presence of a minor G allele is an important protective factor for the development of CHD. Therefore, investigation of SORT1 variations as potential risk modifier genetic factors in Turks may lead to the discovery of better biomarkers for personalized cardiovascular risk assessment.