In chronic myeloid leukemia, resequencing of the BCR-ABL oncogene may direct use of second line inhibitors,11 while in lung cancer, repeat tumor biopsies may identify second site mutations within the driving EGFR and EML4-ALK oncogenes, or therapeutically actionable alterations in other genes capable of bypassing the inhibited cellular signaling, such as c-MET amplification.12 On-treatment tumor sampling in HR+ breast cancer, however, has been limited because many patients harbor only bone metastases, which are not readily amenable to biopsy. This evidence concerns the gene ABL1 and neoplasm.