FGF19 is an important protein in the development and maturation of cartilage and thus a potential treatment target for skeletal metabolic diseases like osteoarthritis. However, it’s not clear how FGF19 regulates cartilage cells (chondrocytes), particularly the mitochondrial changes within these cells. To find out, researchers recently examined FGF19’s role in the formation, fission, and fusion of chondrocyte mitochondria. They found that FGF19 enhanced mitochondria formation (biogenesis) with the aid of the protein β Klotho, which helped FGF19 bind to its receptor. In addition, the enhanced biogenesis was accompanied by increased fusion, which resulted in elongated mitochondria, likely increasing the efficiency of energy production. FGF19 exerted these effects by binding to its receptor FGFR4 on the cell membrane and activating the AMPKα/PGC-1α/SIRT1 signaling axis in a process that was largely dependent on activation of p38 protein signaling. Although the other participating molecules remain to be determined, these findings help clarify how FGF19 regulates mitochondrial dynamics and identify several molecules that could one day be targeted to treat cartilage metabolic diseases.