SMAD2 and hepatocellular carcinoma: Our tgfb1a+ transgenic zebrafish model recapitulated the switch between SMAD and ERK signaling as six weeks of chronic, high tgfb1a induction caused a sharp decrease of P-Smad2+ hepatocytes and a corresponding increase of P-Erk+ hepatocytes, eventually leading to HCC via an Erk-dependent mechanism.