In addition to cancer cell-autonomous effects, activation of oncogenes, such as KRAS and MYC, and inactivation of tumor suppressors, such as TP53, induce transcriptional programs that lead to the establishment of the tumor-promoting microenvironment through the excessive production of pro-inflammatory cytokines and chemokines, recruitment of immune cells, and induction of angiogenesis [30,31,32]. The gene discussed is TP53; the disease is neoplasm.