MME and HIV-associated nephropathy: In HIVAN and collapsing forms of primary FSGS, injured podocytes were found to revert to a developmental program that includes downregulation of cyclin kinase inhibitors, entry into the cell cycle, upregulation of proliferation maker, and loss of mature phenotypic makers, including CD10/CALLA, C3b receptor, GLEPP-1, podocalyxin, synaptopodin, and importantly, WT1 (84–88).