Taken together, our data suggest that the antitumor effects of PTX and NCTD, both individually and in combination, are mediated through a multimodal mechanism involving inhibition of key oncogenic signaling pathways (PI3K/AKT/mTOR and BRAF/ERK), induction of tumor cell differentiation via MITF upregulation, and modulation of transcriptional programs linked to proliferation, metabolism, and stress response. The gene discussed is BRAF; the disease is neoplasm.