In addition, SLE-iPSCs-derived cardiomyocytes exhibited abnormalities, including abnormal sarcomeric structures without filaments, weaker calcium signals, lower proliferation rates, increased hypertrophy, and fibrosis markers protein expression levels induced by the serum derived from SLE patients and anti-Ro autoantibody (164), which suggested that we should pay attention to cardiac and vascular complications leading to death in patients with SLE. Here, CALR is linked to systemic lupus erythematosus.