In patients with fatty liver disease, increased ER stress activates UPR through transducers inositol-requiring enzyme 1, protein kinase R-like kinase, and activating transcription factor 6, which promotes the expression of p53, release of cytochrome C from the mitochondria, and the activation of NF-κB, JNK, and CEBP signaling pathways in KCs, resulting in IR and apoptosis (159, 160). This evidence concerns the gene TBCE and fatty liver disease.