In contrast, APOL1-G1, has reduced binding to APOL1 compared to that of APOL1-G0, and appeared later in response to infections with T. brucei gambiense, which also evolved other mechanisms to block the trypanosomal effects of APOL1-G0 (Cooper et al., 2017; Friedman and Pollak, 2020; Thomson et al., 2014). This evidence concerns the gene APOL1 and infection.