Although p62 upregulation was reported in multiple cancers [41], it is also considered as crucial to cell death: p62 accumulated in Atg5−/− tumor or virus-transformed cells induces DNA damage in response to glucose depletion or oxidative stress [42, 43]; Several anti-tumor drugs promote autophagy-dependent cell death through JNK-mediated p62 expression, showing the increase of both LC3-II and p62 [44–46]. The gene discussed is ATG5; the disease is neoplasm.