If patients with PIK3CA‐ and EGFR‐altered HNSCC tumors are to be candidates for either PI3K or EGFR inhibitors, it may be a relevant therapeutic consideration that a subset of these tumors also have alterations in, or show overexpression of RICTOR and therefore have mTORC2 activity that may continue to drive Akt activation (Janku et al., 2011; Laugier et al., 2015). This evidence concerns the gene EGFR and head and neck squamous cell carcinoma.