The reverse correlation between p62 accumulation and the GFP-LC3 signal that we observed in our in situ tumor analysis suggests that mutations leading to autophagy impairment are likely to be a required oncogenic event that can unleash the pro-tumorigenic function of p62 through Nrf2 overactivation and maybe other signaling pathways [63]. The gene discussed is MAP1LC3A; the disease is neoplasm.