To further explore a potential interaction between inherent, rather than ectopically overexpressed APOL1 and APOL3, and how it might be affected by the presence of the high-risk variants G1 and G2, we conducted co-immunoprecipitation (Co-IP) studies using several cellular systems, including an immortalized human podocyte cell line [92], HepG2 cells, RCC cells and isogenic RCC clones expressing APOL1-null, G1 or G2 variants [93]. Here, APOL3 is linked to renal cell carcinoma.