To better understand the intracellular pathways activated by the constitutively active R137L, R137C, and F229V mutants and how they might translate into the pathological outcome of NSIAD, in this study, we have investigated the phosphorylation pattern of AQP2 in cells expressing the wild-type V2R and its constitutively active mutants R137L, R137C and F229V. The gene discussed is AQP2; the disease is nephrogenic syndrome of inappropriate antidiuresis.