NFKB1 and neoplasm: In addition, several molecular machineries have been proposed to explain the tumor suppressive function of autophagy: (i) accumulation of p62, a substrate of autophagy, leads to NF-κB activation [42]; (ii) accumulation of p62 stabilizes the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), which imparts tumor cells with resistance to hypoxic stress [43]; (iii) retention of damaged organelles, including mitochondria [44].