We further postulate that the beneficial effects of MEK and HDAC inhibitors are mediated at least in part by enhancing cancer cell-intrinsic antigen processing and presentation pathways, potentially enabling CD8 and CD4 T cell recognition of cancer cells through increased MHC class I and II expression and MHC-dependent presentation of a larger, more diverse repertoire of tumor neoantigens. The gene discussed is HDAC9; the disease is cancer.