Since SARS-CoV-2 triggers a massive release of proinflammatory molecules by the immune system (the so-called cytokine storm) [27], increased bone resorption mediated by RANK-RANKL system activation can be expected in COVID-19 patients, and combined with the effects of steroid therapy and prolonged immobilization [10] has the potential to raise the incidence of fragility fractures in patients who have recovered from the infection. The gene discussed is TNFSF11; the disease is COVID-19.