As an example, the use of tyrosine kinase inhibitors for chronic myeloid leukemia can lead to mutations in the BCR-ABL protein (T315I), which confer resistance to the drug [27]; in melanoma, the efficacy of BRAF inhibitor can be abolished by mutations in BRAF or other alternative pathways [28]. This evidence concerns the gene BRAF and chronic myelogenous leukemia, BCR-ABL1 positive.