Furthermore, our data argue that pharmacological inhibition of the NPM1 function could restore the sensitivity of vemurafenib-resistant colon cancer cells with the BRAFV600E mutation by mechanisms that include down-regulation of c-Myc expression and activity and consequent suppression of its transcriptional targets RanBP1 and phosphoserine phosphatase regulating centrosome duplication and serine biosynthesis, respectively. The gene discussed is PSPH; the disease is malignant colon neoplasm.