It is established that autophagy has a tumor-suppressor role and several autophagy gene products including Beclin1 and UVRAG are known to function as tumor suppressor proteins [161] . The tumor-suppressor role of autophagy appears to be important particularly in the liver. Spontaneous tumorigenesis is observed in the livers of mice with either a systemic mosaic deletion of Atg5 or a hepatocytespecific Atg7 deletion [152, 162] . Importantly, no tumors are formed in other organs in Atg5 mosaically deleted mice. Enlarged mitochondria, whose functions are at least partially impaired, accumulate in Atg5-or Atg7-deficient hepatocytes [152, 162] . This observation is in line with the previous data obtained in iBMK cell lines showing that both the oxidative stress and genomic damage responses are activated by loss of autophagy [163, 164] . Again, it is clear that accumulation of p62, at least partially, contributes to tumor growth because the size of the Atg7 −/− liver tumors is reduced by the additional deletion of p62 [162] , which may cause a dysregulation of NF-κB signaling [165] and/or a persistent activation of Nrf2 [166] .