The meta-analysis attributed the efficacy of RASi to two RAS-dependent mechanisms: (1) tumor vascular normalization, where RASi inhibited AT1R-mediated abnormal angiogenesis to enhance drug delivery, and (2) immune modulation, whereby RASi increased CD8+ T cell infiltration, potentially enhancing the response to immune checkpoint inhibitors [120]. Here, AGTR1 is linked to neoplasm.