In this week's PNAS Early Edition, researchers at the Sanford-Burnham Medical Research Institute, along with their collaborators at Columbia University, show that deletion of DDB1 "abrogates the self-renewing capacity of hepatocytes, resulting in compensatory proliferation of DDB1-expressing hepatocytes." In addition, the team shows that "constitutive stimulation of this regeneration process leads to development of hepatocellular carcinoma, which surprisingly contains no disruption of the DDB1 gene." The authors suggest this indicates a "cell-non-autonomous role of DDB1 inactivatio