Despite the impressive hepatocellular swelling due to glycogenosis, the CCF lesions of chREBP-KO mice revealed a significant lower increase of hepatocellular proliferation in association with impeded lipogenesis, contributing to the growth property of AKT/mTOR signaling [20, 22, 25], and in particular of chREBP mediated gene expression alterations [37]. Here, MLXIPL is linked to disorder of glycogen metabolism.