Current evidence supports the view that BCR-ABL1 is the disease-causing mutation in chronic myelogenous leukemia (CML):(i) it is invariably present in CML and absent in other chronic myeloid malignancies; 1 (ii) it induces CML-like disease in mice; 2 and (iii) anti-BCR-ABL1 targeted therapy in CML results in complete and durable hematologic, cytogenetic and molecular remissions. 3 In an ongoing quest to identify BCR-ABL1-like mutations in other myeloproliferative neoplasms (MPNs), scientists have encountered an apparently endless number of mutations involving a spectrum of genes, including