Considering the above observations of Cunin et al. [41], it can be assumed that in the course of autoimmune diseases such as PsA and RA, we are dealing with similar mechanisms of the anti-apoptotic action of CLU, and the elevated CLU concentrations in PsA accompanied by increased sialylation and reduced fucosylation of its glycans may impair CLU anti-apoptotic action. This evidence concerns the gene CLU and rheumatoid arthritis.