AT1R stimulation has been shown to play a role in the differentiation of CD4+ T cells into Th1 cell through the modulation of proteasome function; thus, RASi may inhibit this mechanism of CD4+ T cell antigen-mediated activation.38 The proportion of activated circulating CD4+ T cells may have been diminished as a result of reduced AngII; therefore, trafficking into the liver and tumor was profoundly affected, as it was reported during deoxycorticosterone acetate–salt hypertension.39 The gene discussed is AGTR1; the disease is neoplasm.