Immunosuppressive factors such as TGF‐β, HSP72, and prostaglandin E2 within TEXs impair DC differentiation and maturation by activating STAT3 and downregulating costimulatory molecules.[231] TEXs also induce IL‐6 phosphorylation and reduce MHC class II and TLR4 expression, driving DCs toward a tolerogenic phenotype.[232] Conversely, DCs can internalize TEXs and present tumor‐derived antigens, leading to upregulation of MHC and costimulatory receptors (CD80, CD86), secretion of immunostimulatory cytokines, and T helper cell activation under appropriate conditions.[233]. The gene discussed is HLA-C; the disease is neoplasm.