The exact etiology of SLE remains to be fully delineated; however, most systemic lesions are due to the loss of tolerance to self-antigens, including histone, ribonucleoprotein, double-stranded DNA, antigen Ro (SSA), and antigen La (SSB); direct or indirect damage from autoantibody formation; and the generation of immune complexes (type III hypersensitivity) [20]. Here, CALR is linked to systemic lupus erythematosus.