In recent years, there has been some progress in risk stratification, prevention, and treatment of AKI and the use of the suPAR and other markers of organ damage such as tissue neutrophilic gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule 1 (KIM-1), interleukin 18 (IL 18), inhibitors of metalloproteinase-2 (TIMP-2), and insulin-like growth factor -7 binding protein (IGFBP-7) offer hope for the development of an algorithm to predict the need for KRT in patients with AKI [21,30,31,32]. The gene discussed is CST3; the disease is acute kidney injury.