It has already been shown that DNMT3a mutant HSCs have a selective advantage in surviving high levels of IFN-γ [15], a key upregulated cytokine in malaria infection [26,30,55,56], but repeated, infection-induced bottlenecks in the HSC population may lead to a reduction in HSC clonality even independently of pre-leukemic mutations, and this would inherently affect the robustness of the overall hematopoietic system in the long term. Here, IFNG is linked to infection.