KRAS and neoplasm: Intercellular communication analysis revealed that neutrophils within the tumor microenvironment harboring KRAS and TP53 mutations exhibited significantly enhanced crosstalk with endothelial cells, B cells, macrophages, and epithelial cells compared to those in wild-type settings, particularly through ligand-receptor signaling axes involving oncostatin M, calcitonin receptor, and interleukin 1.