Previous studies have demonstrated that the pharmacologic targeting or silencing of TRIP13 results in the suppression of the Wnt/β-catenin signaling pathway.[17] Wnt/β-catenin activation was frequently associated with poor spontaneous T-cell infiltration across most cancers.[18] We postulated that in addition to directly affecting tumor cells, TRIP13 could also have an immediate effect on the function of immune cells via the activation of Wnt/β-catenin. This evidence concerns the gene TRIP13 and neoplasm.