The intricate interplay within the TRPV4-AT1R complex may provide a potential explanation for the relatively normal blood pressure observed in individuals with peripheral neuropathy diseases resulting from gain-of-function mutations in TRPV4 since activating TRPV4 mutants may be inhibited by the abundant co-expression of AT1R in endothelial cells. The gene discussed is AGTR1; the disease is peripheral neuropathy.