Cytokine-induced disruption of podocyte function, loss of glomerular basement membrane integrity, and reduced ability to retain proteins the size of APOL1, with its predicted molecular weight of 42 kDa, could be the prelude to injury of vulnerable cells by risk variant APOL1 in the glomerular filtrate, even in heterozygous individuals, as observed in patients with HIV-associated nephropathy [57]. The gene discussed is APOL1; the disease is Nephropathy.