However, other members of these pathways include epidermal growth factor receptor (EGFR) that have been implicated with regard to activation in CML41, SRC Proto-Oncogene, Non-Receptor Tyrosine Kinase (SRC) that appears in both GPC-1 and syndecan-3 pathways, whose overexpression have been identified among the known mechanisms of resistance to imatinib in CML42 and FYN proto-oncogene, Src family tyrosine kinase that is up-regulated in CML as result of the BCR-ABL1 oncogene43. This evidence concerns the gene SDC3 and chronic myelogenous leukemia, BCR-ABL1 positive.