Using an inducible KRASG12D/+ construct in PDAC tumor cells containing biallelic loss of TP53, the authors demonstrated that withdrawal of KRAS mutations resulted in a significant reduction in the levels of intratumoral CD11b+ myeloid cells, CD11b+F4/80+ macrophages, and CD11b+CXCR3+ tumor-associated myeloid cells, highlighting the importance of cooperative Ras-p53 mutations in driving innate immune cell recruitment in pancreatic cancer [26]. This evidence concerns the gene KRAS and neoplasm.