Examples include the APOE ε4 and APOL1 gene variants as well as sickle cell disease (SCD) all of which once provided a survival advantage (for instance against malaria in the case of the sickle cell trait (SCT) and against Trypanosoma brucei infections in the case of APOL1) but are now shown to also increase susceptibility to non-communicable diseases [16,17]. This evidence concerns the gene APOL1 and malaria.