Furthermore, BRAF inhibition enhanced drug-induced cell death in BRAF-addicted CRC cell lines and the transfection of a BRAF dominant negative mutant prevented TRAP1 serine phosphorylation, as well as re-establishing drug sensitivity in irinotecan-resistant CRC cells, thus reinforcing the concept that the drug-resistant phenotype of this tumor cell model is addicted to the TRAP1/BRAF reciprocal regulatory mechanism. The gene discussed is BRAF; the disease is neoplasm.