Interestingly, tumors with outlier gene enrichment in EIF2/mTOR also overexpressed genes related to mitochondrial dysfunction, and the tumor (T23) with the most significant enrichment in these three pathways had outlier expression of AKT1 (notable since mitochondrial respiration defects can lead to the activation of AKT-mediated survival [23]; Additional file 2: Figure S3). The gene discussed is AKT1; the disease is neoplasm.