TNKS and neoplasm: Although not further supported by a rescue experiment re-introducing N-terminal mutant β-catenin, the result suggests that loss of WNT/β-catenin signaling in tumor cells is sufficient to trigger a gain of susceptibility and a synergetic relationship to checkpoint inhibition. Nevertheless, we cannot exclude the possibilities that tankyrase inhibition impacts additional biological mechanisms in the tumor cells, in the tumor microenvironment, systemically or on immune cell subpopulations that can contribute to the treatment effect7,19,24,25.