Several mechanisms including induction by specific subsets of DC; expression of specific transcriptional regulators HOBIT, BLIMP, or Runx3; acquisition of integrins; exposure to homeostatic cytokines and inflammatory signals; and improved metabolic fitness have all been implicated in Trm generation and persistence.15 37 41–44 However, most studies have used infectious models, and the relevance of these factors and associated mechanisms for the generation of Trm responses in cancer is less understood. Here, RUNX3 is linked to cancer.