Consistently, auto-Abs against type I IFNs were found in patients with AR NIK or RELB deficiencies, and patients with a specific form of AD NF-κB2 deficiency due to C-terminal variants preventing the cleavage of p100 into p52, resulting in a loss of p52 activity but a gain of inhibitory function for p100 (115). Here, NFKB2 is linked to Alzheimer disease.