We found that PRKCSH overexpression in normal liver cells increases the levels of XBP1 splicing and expression of ER chaperones, leading to resistance to ER stress-induced cell death; whereas PRKCSH silencing sensitizes hepatoma cells to ER stress-induced cell death with downregulation of XBP1 splicing and expression of its downstream target genes. The gene discussed is PRKCSH; the disease is hepatocellular carcinoma.