Cheon et al. (2021) showed that pitavastatin can inhibit RANKL-induced osteoclast formation and function by inhibiting Akt, NF-κB and MAPK signaling pathways, leading to the downregulation of c-Fos and NFATc1, major transcription factors in osteoclastogenesis. In addition, statins act by inhibiting the endogenous synthesis of cholesterol, which is the main substrate for sex hormone synthesis, and Leutner et al. (2019) showed a link between sex hormone levels and statins in the pathogenesis of osteoporosis. This evidence concerns the gene TNFSF11 and osteoporosis.