In this context, other tyrosine kinases have been identified as potential targets of gefitinib and erlotinib, including SYK (32), which predicts a favorable response to fms-like tyrosine kinase 3 (FLT3)-inhibitors in AML patients harboring mutations in the FLT3 gene (33–35), with no EGFR expression. This evidence concerns the gene FLT3 and acute myeloid leukemia.