Due to expression of both CD122 and CD132 receptors involved in cytokine signaling, memory T cells also gain the ability to be activated in the absence of T cell receptor (TCR) triggering and by IL-2 or IL-15 cytokine signaling alone, bypassing the need for TCR engagement in a process called “bystander activation.” This antigen-nonspecific activation can be induced during inflammatory conditions, which is dependent on strong stimuli,such as acute viral infections or cancer immunostimulatory therapies, to maintain function and survival (2–4). The gene discussed is IL2; the disease is cancer.