Furthermore, imatinib is a highly selective ATP-competitive inhibitor of Bcr/Abl, c-KIT and platelet-derived growth factor receptor (PDGFR) [67], but the IC50 ranges considerably amongst different tumour cell lines, since imatinib interacts with non-conserved amino acid residues neighbouring the ATP-binding site [68]. This evidence concerns the gene PDGFRB and neoplasm.