Recently, it has been demonstrated that the use of tolvaptan doses, likely to be attained in the plasma of ADPKD patients, inhibited AVP-induced proliferation through the B-Raf/MEK/ERK pathway and decreased both AVP-stimulated chlorine secretion and in vitro cyst growth of ADPKD cells [125]. Here, BRAF is linked to autosomal dominant polycystic kidney disease.