Studies by the Evan group have shown that inhibiting endogenous murine c-Myc in vivo through an inducible dominant negative c-Myc protein (OMOMYC) causes regression of a variety of murine tumours (including lung tumours induced by Kras mutation and pancreatic neuroendocrine tumours in mice carrying the Riptag transgene).16, 17 Moreover, the effects of c-Myc loss were well-tolerated suggesting that c-Myc is an attractive therapeutic target. The gene discussed is MYC; the disease is neoplasm.