In the cancer scenario, AT1R activation by AngII favors cell proliferation, inhibits apoptosis, and promotes adhesion molecule expression, the interaction of monocytes with endothelial cells (EC), the infiltration of inflammatory cells, and the generation of pro-inflammatory cytokines, enabling the establishment of the inflammatory microenvironment, which is a pivotal state for the subsistence of neoplastic cells [47]. This evidence concerns the gene AGTR1 and cancer.