In a study exploring the mechanisms of myocardial fibrosis, it was mentioned that Calreticulin overexpression in the endoplasmic reticulum caused disruption of Ca2+ homeostasis, transient activation of the unfolded protein response (UPR)-IRE1a pathway was shown to be a key factor in cardiac fibrosis, and administration of an inhibitor of the UPR was shown to be effective in blocking IRE1α activity and reduced the splicing of XBP1 (Groenendyk et al., 2016). This evidence concerns the gene CALR and Myocardial fibrosis.