The demonstration that the APOL1 inhibitor VX-147 prevents both APOL1 variant-induced toxicity and K+ fluxes [32] does not prove that APOL1 variant-driven cationic pore formation is responsible for kidney disease, because VX-147 has not been demonstrated to specifically block the APOL1 pore, but could alternatively interfere with APOL1 folding, interactions and/or stability, inhibiting other processes affected by APOL1 variants. Here, APOL1 is linked to kidney disorder.