DNMT1 and neoplasm: Ezh2, a member of the polycomb repressive complex 2 (PRC2) and Dnmt1, a DNA methylation enzyme were most highly expressed in the B16F10 model (Additional file 2: Figure S7), implicating both β-catenin pathway activation and epigenetic silencing as potential tumor intrinsic mechanisms leading to resistance to checkpoint inhibitors in this model.