A crucial by-product of oncogene suppression in CML is that SCN-adapted cells are refractory to the tyrosine kinase inhibitors (TKi) which target the constitutive enzymatic activity of the BCR/Abl oncogenic protein responsible for disease [33, 35], in keeping with findings obtained in other laboratories [36–38]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.