Studies have shown that MA could suppress N‐myristoyl‐transferase, a critical enzyme involved in Src myristicylation26 to endoplasmic membrane and further phosphorylation.25 MA‐induced Src inhibition then affects a large number of cytoskeletal changes in osteoclasts, reduces latter stages of osteoclast differentiation and prevents RANKL‐induced bone loss in vivo.25 Such inhibitory effects against osteoclast formation and function suggest MA might serve as a new therapeutic agent against osteolytic bone disorders. The gene discussed is SRC; the disease is bone disorder.