CD8A and neoplasm: Agonistic antibodies or GITR ligand binding to GITR in concert with T cell receptor (TCR) stimulation causes activation of the MAPK/ERK pathway and NFkB, resulting in augmentation of T cell proliferation and proinflammatory cytokine production and enhanced anti-tumor effector function [5, 6], as well as resistance of CD4+ and CD8+ T cells to Treg suppression [4].