While each parasitic infection induces a distinct immune program, several recurring sex‐biased patterns have emerged: males tend to exhibit heightened Th17‐mediated activity in amebiasis and leishmaniasis, whereas females mount stronger IFNγ and IFN‐mediated responses and show higher ISG expression across amebiasis, leishmaniasis, and malaria, along with increased IL‐10 production in malaria and schistosomiasis (Figure 2). The gene discussed is IFNG; the disease is leishmaniasis.