The defects range from defects in the proteasome in both the non-obese diabetic (NOD) mouse model and humans with Sjogren’s syndrome, to specific polymorphisms in the TNFR1 or TNFR2 receptors themselves, to punitive interruptions in genes that control the ubiquitination of the NFkB pathway. This evidence concerns the gene NFKB1 and Sjogren syndrome.