The dysregulation of these pathways is very common in many cancer types: Receptor Tyrosine Kinases (RTKs) amplification and mutations, PIK3CA or Ras mutations, and loss-of-function mutations in negative regulators such as PTEN, collaborate to constitutively activate either PI3K/Akt or Ras/ERK signaling coupled to mTOR signaling. The gene discussed is AKT1; the disease is cancer.