While often the basis for human infectivity in such infections has not been able to be fully investigated, T. b. evansi infections have been identified to occur both in an individual lacking APoL1 due to null mutations [155], but also recently in a patient with no observable ApoL1 deficiency [156], suggesting there remain aspects yet to be explained in this intensively studied and important host-parasite interaction. The gene discussed is APOL1; the disease is infection.