Additionally, activation of type 1 angiotensin II receptors (AT1R) in the RAAS may benefit the establishment of a tumorigenic microenvironment, and ACEIs/ARBs, as RAAS inhibitors, are likely to inhibit expressions of vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-7, tumor-associated macrophages, and c-myc [39]. Here, MYC is linked to neoplasm.