Preclinical studies suggest that oncogenic BRAF (BRAF V600E) may contribute to immune escape in melanoma [18], and that blocking its activity via MAPK inhibition leads to increased expression of melanocytic differentiation antigens (MDAs) [19, 20] with significantly enhanced recognition by antigen-specific T lymphocytes [20, 21], enhanced antigen presentation [22, 23], without diminishing T-cell function [24], and change in the tumor-produced immune environment [25]. This evidence concerns the gene BRAF and neoplasm.