Prompted by the findings that resistant BRAF-mutated colon cancer cells exposed to cytotoxic doses of PLX4032 express an increased activity of nucleophosmin associated with the promotion of centrosome duplication concomitant with an increased stability and activity of its binding partner, c-Myc, we sought to further investigate whether pharmacological targeting of NPM1 and c-Myc could increase the efficacy of PLX4032 in resistant cell lines. The gene discussed is BRAF; the disease is colonic neoplasm.