However, ICC lesions eventually occurred in all mouse livers depleted of Notch1. In striking contrast, when Notch2 was knocked-out in hepatocytes, not only it led to delayed tumor development, but also resulted in the exclusive formation of hepatocellular adenoma and HCC-like lesions, thus recapitulating the phenotype observed following the inhibition of the canonical Notch signaling. The gene discussed is NOTCH2; the disease is neoplasm.