The original report investigating mutated PIK3CA led to hyperactivation of the PI3K-AKT-mTOR pathway in SCC derived from oral squamous cell carcinoma (OSCC) [26], wherein AKT was found to be highly phosphorylated in OSCC cell lines with PIK3CA mutations compared to that in their counterparts without mutations. This evidence concerns the gene AKT1 and oral cavity squamous cell carcinoma.