This tumor also showed additional mutations such as amplification of TP63, SOX2, PIK3CA, FADD, CTTN, CCND1, EGFR, FGFR1, CASP8, SMAD4, TP53, NFE2L2, NOTCH1, 2,& 3, MYC, PTK2, AJUBA, TRAF3, ERBB2, NRAS, KRAS, HRAS, FAT1, KEAP1, E2F1, and SMAD2, loss of RASSF1, FHIT, CDKN2A, KMT2D, RB1, APC, CSMD1, PTPRD, MET, CUL3, and NSD1 and a LOH of TP53, NOTCH1, APC, RB1, CSMD1, PTPRD, CUL3, NSD1, CDKN2A, FHIT, and RASSF1, which have been reported in HNCSS (1, 13, 25). This evidence concerns the gene SMAD4 and neoplasm.