TSC1 and neoplasm: ,24,25 In this mouse model, constitutively high mTOR signaling due to liver-specific double knockout of the tumor suppressors TSC1 and PTEN (hereafter referred to as L-dKO) drives the sequential development of hepatomegaly, hepatosteatosis, steatohepatitis, and multiple high-grade HCC within 20 weeks of age.23