Other studies seem to support these findings: cells expressing distinct mutant BRAF splice variants grew more efficiently in vitro and in vivo in the presence rather than in the absence of the vemurafenib analog PLX4720 and, after a drug free interval, became re-sensitized to BRAF inhibition; a drug holiday was also shown to be effective in a melanoma cell line in which resistance was mediated by BRAF copy number amplification [77] and acquired EGFR expression [36]. This evidence concerns the gene BRAF and melanoma.