CD8A and neoplasm: As a confirmation of the negative impact of the KRAS-G12D mutation on the immune responsiveness, inhibition of such mutant protein with MRTX1133, a specific small molecule inhibitor of KRAS-G12D variant, has been reported to somehow revert the immune suppressive status of TME by increasing the intra-tumor infiltrate of CD8+ effector T cells and contributing to make PDAC more immunogenic and better reactive to immunotherapy [47–49].