Our findings are also consistent with work in other tumor and non-tumor models demonstrating a role for FOXC2 in the activation of PI3K-Akt-mTOR signaling (5, 20, 21), as we found that several genes associated with the PI3K-Akt signaling pathway (mmu04151) and the mTOR signaling pathway (mmu04150) were upregulated in B16-F1 as compared to its FOXC2-deficient counterpart. This evidence concerns the gene MTOR and neoplasm.