With regard to FOXC2's well-established role in promoting chemotherapy resistance in tumor cells (14, 15, 19, 20), our data suggests potential mechanisms by which this chemoresistance may be achieved, including induction of genes associated with drug metabolism such as the carbonyl reductase gene Cbr3, the oxidoreductase gene Nqo1, the cytochrome P450 family member Cyp26b1, and several members belonging to the glutathione S-transferase gene family (which fall outside of the top 30 upregulated genes shown in Table 1). This evidence concerns the gene FOXC2 and neoplasm.