We conducted gene expression profiling and pathway analysis of microarray data generated from a prior gefitinib versus M4-AML study. The previous study was conducted by the Broad Institute of MIT/Harvard. In that study, RNA was extracted from primary patient-derived cells and examined using Affymetrix ^® microarray technology. In our secondary analysis of the data, over 14,500 genes were examined for p-value and fold-change using four bioinformatics programs. Our findings indicate that a therapeutic reduction of the myc oncoprotein correlated to molecular reversal of cell transformation within 24 hours of treatment. We analyzed the known efficacies of gefitinib and were able to identify a bona fide gefitinib target in the PDGFR pathway that we believe to be responsible for tumor regression. This target, SRC, demonstrated moderate interactions with gefitinib in small molecule/tyrosine kinase binding assays and has proven critical to MYC induction in gene inhibition assays.