Phenotypically, STAT3‐deficient mice exhibit impaired Th17 differentiation, defective humoral immunity and increased susceptibility to infection, partly due to loss of IL‐21 induction and impaired RORγt and IL‐23R expression—key STAT3‐dependent signals essential for Th17 lineage commitment and function [7, 8, 9]. This evidence concerns the gene STAT3 and infection.