It is known for some time that certain human leukocyte antigen (HLA) class II molecule variants favor B-cell responses to the anti-Sjögren’s-syndrome-related A (Ro/SSA) and anti-Sjögren’s-syndrome-related B (La/SSB) autoantigens, formation of lymphocytic infiltrates with germinal centers, and risks for MALT lymphomas and vasculitides, evidently because the high-risk HLA class II variants have high affinities for Ro/SSA and La/SSB epitopes [5,6,7]. This evidence concerns the gene CALR and MALT lymphoma.