This exhaustion is characterized by reduced effector cytokines and cytolytic molecules, coupled with upregulation of inhibitory immune checkpoint proteins such as lymphocyte activation gene 3 (LAG‐3), T‐cell immunoglobulin and mucin domain 3 (TIM‐3), and PD‐1, as well as their interaction with galectin‐9.[5] Therefore, identifying barriers within the TME that impede T‐cell function is crucial to enhancing the effectiveness of T‐cell‐based cancer immunotherapies. This evidence concerns the gene PDCD1 and cancer.