Chu and collaborators have showed the implication of ventricular fibroblasts in the development of a drug-induced Long QT syndrome (LQTS) by demonstrating that transforming growth factor β (TGF-β) produced by fibroblasts induced a down-regulation of Kv11.1 (hERG) and Kir2.1 K+ channels expression in cardiomyocytes6. Here, KCNH2 is linked to familial long QT syndrome.