Anti‐PD1 and anti‐CD137 mAb act on T cells that express these receptors on their plasma membrane presumably as a consequence of an antigencognate activation process. Hence, the main mechanism of action is exerted on tumor infiltrating lymphocytes that express such receptors on their surface, thus becoming amenable to pharmacological modulation with the corresponding mAb. In preclinical mouse models, anti‐CD137 and anti‐PD1 mAbs exert powerful synergistic effects. The gene discussed is TNFRSF9; the disease is neoplasm.