It is crucial to prevent the T cell exhaustion through blockade of multiple immune checkpoints for improving the efficacy of tumor immunotherapy.[25, 26] For example, Hung et al. used anti‐galectin‐9 (Gal‐9) antibody and agonistic antibody (DTA‐1) to co‐stimulate GITR (glucocorticoid‐induced tumor necrosis factor receptor‐related protein) receptor to reduce the expression of PD‐1 and TIM‐3 on T cells and enhance immunotherapy.[27]. The gene discussed is PDCD1; the disease is neoplasm.