By demonstrating that JAK/STAT signaling is the central mediator of these combined cytokine effects, our results provide a plausible explanation for how the COVID-19 cytokine storm drives APOL1 expression and the high incidence of collapsing glomerulopathy seen in patients with risk-variant APOL1 and COVID-19 infection. The gene discussed is SOAT1; the disease is COVID-19.