More commonly, however, cancers were found to overcome MTOR inhibition by activation of other oncogenic pathways, including overexpression of MYC[210], IDO1[211], other components of the AKT pathway[212], or rebound activation of AKT[213,214], such as through MTORC2 activity (not inhibited by current MTOR inhibitors)[215-217]. This evidence concerns the gene MTOR and cancer.