CD4 and neoplasm: The potential approaches may include Treg depletion, attenuation of Treg immunosuppressive functions, prevention of Treg homing at the tumor sites, and exploitation of T-cell plasticity (e.g., blocking conversion of conventional CD4+ T cells into induced Tregs or reprogramming “terminally differentiated” Tregs toward effector T cell subsets, such as TH17) [25].