Moreover, the KRAS-G12D mutation occurs in nearly half of PDAC patients and its oncogenic signaling has been reported to contribute in maintaining the immune evasive status of the tumor microenvironment (TME) in such cancer type [39, 40], by also suppressing PD-L1 expression, thus impairing the activity of immune checkpoint inhibitors (ICIs) in PDAC and explaining the observed low response of PDAC to immunotherapy [41–43]. This evidence concerns the gene KRAS and neoplasm.