In this week's PNAS Early Edition, researchers at the Cold Spring Harbor Laboratory in New York and their collaborators present evidence to suggest that "large cancer-associated deletions can produce phenotypes distinct from those arising through loss of a single TSG [tumor-suppressor gene], and as such should be considered and studied as distinct mutational events." The team tested its hypothesis — that large chromosomal deletions "can arise from selective pressure to attenuate the activity of multiple genes" — in a murine model of hepatocellular carcinoma using in vivo R