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. This evidence concerns the gene NPM1 and colonic neoplasm.