CTLA4 and cancer: Na Kwon Joong et al reported the ratio of GLUT3 and GLUT1, a surrogate of the reciprocal glucose metabolic activity between cancer and immune cells, predicts good immunotherapy response (anti-PD1 and anti-CTLA4).66 However, Renner Kathrin et al reported restricting glycolysis preserved T cell effector functions and augments checkpoint therapy.67 More mechanistic studies are expected to further elucidate the causes of drug resistance to anti-PD1 therapy.