CD4+ Th1 cells from cervical carcinoma stimulate the tumor-rejection environment by converting M2 macrophages into classical proinflammatory M1 macrophages via prostaglandin E2 and IL-6,[40] and the maintaining efficacious tumor-associated macrophage depletion is an effective anticancer therapy for cervical cancer.[41] Cytokines involved in inflammatory processes and various functions have attracted the attention of researchers. Here, CD4 is linked to neoplasm.