In follicular lymphoma tumors, IL-4 produced by T_FH binds to its receptor (IL-4R) on tumor cells and leads to activation of Jak1 and Jak3, which, in turn, results in phosphorylation, dimerization, and translocation of STAT6 to the nucleus. Phosphorylated STAT6 induces genes that may promote survival and proliferation of the tumor cells and also stimulates production of CCL17, which facilitates recruitment of immunosuppressive regulatory T cells (Tregs) via CCR4. Compared with wild-type (wt) STAT6 (STAT6_WT) (A), mutant STAT6 (STAT6_mu) (B) results in increased localization of STAT6 to the nucleus, especially in the presence of IL-4, and leads to increased expression of genes, including those that might promote survival and proliferation and facilitate immune evasion.