Interestingly, a recent study related to chronic pancreatitis reported that hypoxia and HIF‐1α activation in the pancreas are crucial for the activation of pancreatic stellate cells and the development of pancreatic fibrosis.[50] Through assessments of cell‐cell interactions, we also established that HIF1A+ classic monocytes are vital effector cells interacting closely with pancreatic stellate cells, with visfatin playing a significant role in this process across both types of AIP. This evidence concerns the gene HIF1A and autoimmune pancreatitis.