Recent evidence demonstrates that an antisense oligonucleotide of APOL1 efficiently protects against IFN-γ-induced proteinuria in APOL1-G1 transgenic mice [68], indicating that APOL1-induced M1 macrophage secretion of interferon -γ, M1 polarization and subsequent pro-inflammatory immune responses play at least partial roles in the APOL1-associated CKD. The gene discussed is APOL1; the disease is chronic kidney disease.