As shown in Supplementary Fig. S6, expression remains relatively similar compared to levels in control cells, and thus reduction in PTEN is unlikely to explain the elevated AKT activity, with the caveat that PTEN function can be lost through mutation, although relatively rare in HNSCC.48 Taken together, the data suggest that, while blockade of EPS8 phosphorylation by Src may downregulate cell cycle-related and other genes important for proliferation in cell culture, there is concomitant upregulation of other genes, the products of which may serve to promote tumorigenesis in vivo. This evidence concerns the gene PTEN and head and neck squamous cell carcinoma.