BRAF and melanoma: The class I and II HDAC inhibitor, trichostatin A, has often been applied for mechanistic investigations, and a transcriptomic study in BRAF-mutant melanoma cells revealed downregulation of transcripts involved in the promotion of the BRAF-ERK1/2 pathway (e.g., protein kinase C δ upstream of BRAF, and MYC proto-oncogene downstream of BRAF) upon treatment with trichostatin A[46].