ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive: The authors thus postulated that i) physiologic BCR-ABL1 expression may be insufficient for development of a CML-like disease; ii) in the retroviral or transgenic models, non-physiologic, very high levels of BCR-ABL1 expression due to multiple copies of the oncogene and expression from a very active retroviral promoter, non-specificity of expression timing and locale and maybe also random insertion-site mutations could artificially select for disease development [31].