Using paired-end DNA sequencing, Ng et al.[89] (2012) discovered an intronic deletion polymorphism in BIM that was sufficient to confer intrinsic resistance to the tyrosine kinase inhibitors, imatinib and gefitinib in chronic myeloid leukemia (CML) and epidermal growth factor receptor-mutated non-small-cell lung cancer (EGFR NSCLC). Here, EGFR is linked to chronic myelogenous leukemia, BCR-ABL1 positive.