Additionally, three patients harbored mutations in both BRAF and NRAS; 10 patients exhibited dinucleotide polymorphisms (DNPs) in BRAF, and one DNP was identified in NRAS. Further analysis revealed a number of truncation mutations in well-established tumor suppressors (TP53 and RB1), protein phosphatase genes (e.g., PTEN, PTPRB, PTPRD, PTPRN2, PTPRT, and PPP1R3A), and chromatin remodeling genes (e.g., ASXL3, MLL2, and ARID2) (Figure S2 in File S1). Here, PTPRD is linked to neoplasm.