This tumor showed mosaicism in the amplification of TP63, PIK3CA, SOX2, FADD, CTTN, CCND1, NOTCH1, E2F1, HRAS, BIRC2, EGFR, MYC, PTK2, loss in FHIT and CDKN2A, and LOH in NSD1, FAT1 and APC. All these mutations constitute a combination of distinct mutation profiles for various molecular sub-types of HNSCC of different etiology (1, 13, 25). This evidence concerns the gene NSD1 and neoplasm.