In this issue of Genes & Development, Wei and colleagues (pp. 1204-1216) use elegant genetic approaches to simultaneously delete the essential autophagy gene FIP200 (FAK family-interacting protein of 200 kDa) and the signaling adaptor p62/SQSTM1 within established murine tumors, which reveals an unexpected synergism between the autophagy pathway and p62 in driving tumor growth. Intriguingly, these observations suggest that the combined targeting of autophagy and p62 may serve as an effective approach to treat specific cancers
