Furthermore, while in chronic myeloid cancers, such as BCR-ABL-negative MPNs, the main molecular basis is represented by mutations in Janus kinase 2 (JAK2) or cytokine receptors leading to constitutive JAK-signal transducer and activator of transcription (STAT) signalling [45], in secondary leukaemia and in the more severe MPN, many more mutations, especially in epigenetic regulators and genes coding for transcription factors, have been identified[6]. The gene discussed is ABL1; the disease is leukemia.