The specific mechanisms whereby the APOL1 risk variants increase the risk for renal disease are not fully understood, but beyond their role in innate immunity and resistance to trypanosomiasis, the APOL1 risk variants are considered gain-of-injury variants (Kruzel-Davila et al., 2016), intensifying autophagy, cell death, endothelial cell inflammation and dysfunction, and immune pathway activation (Wu et al., 2021; Friedman and Pollak, 2020; Daneshpajouhnejad et al., 2022). Here, APOL1 is linked to kidney disorder.