Whereas another APOL1-G1 BAC (C57BL/6 background) mouse model developed proteinuria following injection with recombinant IFN-γ, it did not develop FSGS-like disease, probably due to the transient increase in APOL1 expression (Aghajan et al., 2019). This evidence concerns the gene IFNG and focal segmental glomerulosclerosis.