Although this interesting non-proteolytic function of SKP2 has been characterized in breast carcinoma, it is reasonable to expect that the SKP2-AKT circuit may represent an alternative way to hyperactivate the AKT oncogenic signaling in those SCCs not harboring oncogenic mutation of PI3K and/or amplification of its upstream regulators (i.e., EGF-R). The gene discussed is SKP2; the disease is breast carcinoma.