Pathway analyses using a combined set of single-nucleotide and copy number data across the whole cohort of cervical carcinomas revealed that ERBB- and PI3K/AKT/mTOR signaling were enhanced within mutated and/or amplified oncogenes (Supplementary Table 8), while p53 signaling and interferon signaling were enriched among deleted and mutated tumor suppressors (Supplementary Table 9). The gene discussed is AKT1; the disease is cervical carcinoma.