This contrasted with the phenotypes observed with the ALL-derived etv6-jak2a fusion, with the functional differences correlating with increased activation of the downstream STAT transcription factors by the atypical CML-derived etv6-jak2a fusion that also showed enhanced sensitivity to JAK2 inhibitors [78]. This evidence concerns the gene ETV6 and chronic myelogenous leukemia, BCR-ABL1 positive.