SOAT1 and lipoprotein glomerulopathy: 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.