While APOL1 variants confer protection from sleeping sickness, high-risk genotypes (G1-G1, G1-G2, G2-G2) increase the risk of developing glomerulosclerosis, as demonstrated by transgenic mice with podocyte-specific expression of APOL1 G1/G2 alleles which develop proteinuria, foot process effacement, and FSGS. This evidence concerns the gene APOL1 and focal segmental glomerulosclerosis.