HMGB1 and adenoma: Our findings support the following conclusions: (1) The adenoma originates from the autophagy-deficient hepatocytes; (2) Hepatocyte-derived HMGB1 stimulates tumor cell proliferation; (3) HMGB1 mediates the proliferative signal at least in part via RAGE in a paracrine mode; and (4) Tumors developed in the presence or absence of HMGB1 have significantly different transcriptomic profiles and mitochondria function could be an important mechanistic linker to tumor promotion.