Several transgenic mouse models have been developed to study APOL1-nephropathy, but none of these models develop both the proteinuria and the histologic lesions observed in humans in response to a known trigger (Beckerman et al., 2017; Bruggeman et al., 2016; Okamoto et al., 2018; Kang et al., 2018; Aghajan et al., 2019; Kumar et al., 2018). The gene discussed is APOL1; the disease is kidney disorder.