Osteoporosis commonly caused by enhanced pathological bone resorption or bone loss because of the increased OCs activation.24 Previous study proved excessive OCs differentiation (osteoclastogenesis) is mostly via the classic signalling pathway: RANKL, which has been a potential valuable target for treating osteoporosis.5 Our current study of myricitrin down‐regulation effects on osteoclastogenesis and decreased mature OC's bone resorptive function have demonstrated myricitrin as a natural inhibitor, possessing therapeutic potential on treating pathological bone loss disease. Here, TNFSF11 is linked to osteoporosis.