Hence, mitigating RANKL using denosumab may reduce subacute inflammation and improve insulin resistance.11,36 Another hypothesized mechanism is that RANKL suppression may promote β-cell proliferation.37 The failure of β cells is a fundamental pathogenic process in diabetes.38 Since the RANKL/RANK pathway inhibits β-cell replication in humans, suppressing the RANKL/RANK pathway via denosumab may enhance human β-cell replication.37 Such compelling evidence suggests potential underlying mechanisms for the association between denosumab and preventing diabetes development. This evidence concerns the gene TNFRSF11A and diabetes mellitus.