In conclusion, the effect of APOL1 variants on cation fluxes, considered responsible for the major cytopathology induced by these variants either in cultured cells in vitro or upon infection-linked inflammation in vivo, is unlikely to result from the formation of APOL1 channels at the podocyte surface but more likely reflects the activation of other channels in the podocyte plasma membrane. Here, APOL1 is linked to infection.