By utilizing our approach, we were able to detect dysregulation of the major molecular processes involved in HNSCC tumorigenesis (such as those involving PI3K/AKT/mTOR, RAS/RAF/MAPK, JAK/STAT, WNT/β-catenin and TGFβ/SMAD signaling) in almost every OSCC tumor analyzed. This evidence concerns the gene SOAT1 and neoplasm.