Moreover, since p300 activity can be regulated by MAPK signaling (Chen et al., 2007), the greatly enhanced tumor-forming capacity observed with the MITF K243Q mutant compared to K243R further suggests that transcription factor acetylation driven by activated oncogenes like BRAF will fuel proliferation in cancer in part by releasing transcription factors from their genomic reservoir. This evidence concerns the gene MITF and neoplasm.