However, deletions of the human 1p36 region identified for several hematopoietic malignancies, including acute AML [8], CML [9] and non-Hodgkin’s lymphoma [10], did not include CHD5. Although this does not support CHD5 deficiency as a causal event in these cancers, the finding that mice heterozygous for the 4.3-Mb interval encompassing Chd5 are prone to spontaneous lymphoma [35] and that CHD5 is deleted in lymphoid cancers in mice provide evidence that CHD5 deficiency plays a key role in these hematopoietic malignancies [39]. This evidence concerns the gene CHD5 and chronic myelogenous leukemia, BCR-ABL1 positive.