In physiological conditions, the expression of both isoforms is sufficient to maintain PRL synthesis and secretion and cell proliferation, while the simultaneous knockdown of both D2DR isoforms induces the inhibition of ERK1/2 and the induction of PKB activity resulting in uncontrolled cell proliferation and consequent pituitary hyperplasia and hyperprolactinemia (35). This evidence concerns the gene PRL and hyperprolactinemia.