Nevertheless, the activation of WNT/β-catenin signaling pathway—including the downstream WNT effectors CTNNB1 and APC, which were found mutated in a large fraction (22/55; 40%) of PDAC cases in our series—is another critical molecular mechanism for pancreatic tumor initiation and progression as well as for facilitating immune evasion and contributing to immunotherapy resistance of such a tumor [53]. Here, CTNNB1 is linked to pancreatic neoplasm.