Bereshchenko and coworkers demonstrated that mutations in the C/EBPα protein efficiently drive leukaemia in vivo and that the combination of N- and C-terminal mutations were the most highly leukaemogenic, whereas biallelic C-terminal mutation resulted in the longest latency (Kirstetter et al, 2008; Bereshchenko et al, 2009). The gene discussed is CEBPA; the disease is leukemia.