Strikingly, we found a significantly more severe nephropathy phenotype in an anemic context as indicated by accelerated dextran clearance, with co-suppression of apol1 and myh9 under atpif1α-MO induced anemia (n = 12–19 embryos/injection; p<0.001 for myh9/apol1 MOs vs. myh9/apol1/atpif1a MOs; Fig 5C and 5E). This evidence concerns the gene APOL1 and kidney disorder.