APEX1 and cancer: Hyperactivation of IL6/STAT3 signaling in both dysplastic and EAC tissues has been linked to JAK–STAT3–mediated promotion of cancer cell survival in response to bile acid treatment through BCL-XL116 and MCL1126 levels, which may also be p53-dependent; however, induction of STAT3 signaling also has been observed to be mediated additionally through an epidermal growth factor receptor and Apurinic/apyrimidinic endonuclease-1 (APE1)–mediated axis in a redox-dependent manner.136