The circulating level of anti-mCRP autoantibodies in patients with lupus nephritis (LN) was closely associated with the score of their interstitial lesions.[18] Recently, Li et al[19] showed that a.a. 35 to 47, a sequence exposed only in mCRP, constitutes the major epitope recognized by anti-CRP autoantibodies in patients with LN and indicates that mCRP binds complement factor H and enhances its cofactor activity via a.a. 35 to 47, whereas autoantibodies against this epitope inhibit these actions and adversely affect LN. This evidence concerns the gene CRP and lobular neoplasia.