In a similar way, Liu et al. [89] have also found that Bmal1 is able to protect against experimental acute pancreatitis through blocking the ferroptosis-mediated release of HMGB1, a mediator of sterile inflammation, while promoting the expression of multiple antioxidant or membrane repair systems, thereby suppressing ferroptosis-mediated damage in pancreatic tissue. This evidence concerns the gene HMGB1 and acute pancreatitis.