Because cytology reveals tumor heterogeneity at the single cell level, researchers were able to recognize the driving mutation in CML (the BCR-ABL gene fusion) [55], [57], develop a successful drug (imatanib) to target that lesion [58], observe the selective effects of imatanib treatment [59], [60] and, with that knowledge in hand, develop second-line drugs (e.g., dasatinib) that work on imatanib- resistant CML [22], [61]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.