Pharmacological inhibition of NPM (nucleophosmin) effectively restored the susceptibility of vemurafenib-resistant BRAF-mutated CRC cells by down-regulating the expression and activity of c-Myc and consequently suppressing its transcriptional targets: RANBP1 and phosphoserine-phosphatase, that regulate centrosome duplication and serine biosynthesis, respectively [64]. Here, RANBP1 is linked to colorectal carcinoma.