Previous studies have revealed that an increase in NF-κB-p65 phosphorylation promotes the secretion of a series of inflammatory cytokines in OVX-induced mice or postmenopausal osteoporosis patients.41,42 Given the fundamental role of Trim21 in regulating immunity via ubiquitination of the nuclear factor‐κB p65 subunit,30,43 it would be interesting to further determine whether the regulation of Trim21 in bone metabolism can partially be attributed to the mediation of immunity. This evidence concerns the gene NFKB1 and postmenopausal osteoporosis.