PPIB and metabolic dysfunction-associated steatohepatitis: Further analysis revealed that suppression of endoplasmic reticulum (ER) stress by lowering glucose-regulated protein 78, phosphorylated eukaryotic translation initiation factor 2α, and phosphorylated c-Jun N-terminal kinase while increasing ER-resident protein 57, phosphorylated Ak strain transforming and phosphorylated mitogen-activated protein kinase was a possible bioactivity mechanism of baker’s yeast β-glucan in NASH prevention [45].