Our findings are in line with reports of RAS-MAPK signaling reactivation through the loss of NF1 as a mechanism of resistance to other targeted therapies, including EGFR inhibition in lung cancer [58], BRAF inhibition in melanoma [59], BCR-ABL inhibition in chronic myeloid leukemia [60] and endocrine therapies in advanced breast cancer [61]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.