In organ cultures of prostate cancer, in which Stat5a/b-mediates epithelial-to-mesenchymal transition (EMT) (epithelial-mesenchyme transition), disruption of Jak2/Stat5a/b signaling by specific inhibitors resulted in a significant decrease in active nuclear Stat5a/b but not Stat3, increase levels in E-cadherin and simultaneously a decrease in levels of Twist1 indicating that active Stat5a/b signaling promotes expression of EMT markers (48). Here, STAT5A is linked to prostate carcinoma.