Thus, the key to reconciling the apparent contradiction between generally decreased—compared to non‐ACLF patients with CLIF‐C AD scores ≥ 50—and mortality‐associated increased sIgA levels in ACLF lies in understanding the three‐step process leading to sIgA appearance in circulation: (1) mucosal IgA production, (2) active secretion into the intestinal lumen via the polymeric‐Ig receptor (i.e., binding with the secretory component) and (3) subsequent translocation from the lumen back into circulation. Here, CD79A is linked to Alzheimer disease.