Evidence from in vitro and in vivo studies indicate that BRAF inhibitors do this by increasing the expression of melanoma differentiation antigens, such as melanoma antigen recognised by T cells (MART-1), glycoprotein 100 (gp100), tyrosinase-related protein-1 (TYRP-1), TYRP-2 and dopachrome tautomerase (DCT) on BRAF-mutant cells [37,46], and also by increasing the expression of HLA 1 on the surface of BRAF-mutant melanoma cells [22,35]. The gene discussed is PMEL; the disease is melanoma.