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In recent years, the number of new mechanisms and molecular targets of SFN in the treatment of fatty liver reported by experimental studies has increased rapidly (Figure 1), such as inhibition of lipogenic enzymes via ER stress-dependent decrease of X-box binding protein 1 (XBP1) expression and ER stress-independent blocking of sterol regulatory element binding protein-1c (SREBP1c) pathways (Tian et al., 2018a), alleviated ER stress through the upregulation of AMPK and peroxisome proliferators-activated receptor (PPAR) ( in vitro and in vivo (Tian et al., 2021b)