Multiple myeloma (MM) is a B-lymphocyte-derived malignancy characterized by a monoclonal proliferation of plasma cells that produce a clonal immunoglobulin. Monoclonal gammopathy of undetermined significance (MGUS) is an asymptomatic precursor condition commonly preceding MM.(1) Recent studies show that family members of MGUS and MM patients have a two to threefold higher risk of developing MGUS/MM.(2,3) Environmental influences, chance occurrence, and inherited factors might all contribute to familial clusters. Also, the incidence of MM and the prevalence of MGUS are reportedly two to threefold higher among Black people than White people,(4–6) and lower in Asians.(6,7) Until now, the pathogenesis of MGUS/MM has remained obscure. A causal relationship between MGUS/MM and chronic antigenic stimulation has been suggested by the results of several studies,(8–12) hence the identification of the antigenic stimuli of B-cell neoplasms might be of considerable importance. Antigenic targets of paraproteins were discovered accidentally due to clinical symptoms caused by the paraprotein (e.g. chronic cold agglutinin disease or cryoglobulinemia(13) or bleeding disorders(14)), because of interference of the paraprotein with laboratory tests ordered for the clinical work-up of the patient (e.g. HIV-1 p24 antigen in an HIV-infected patient with myeloma),(15) and/or by screening paraproteins against pre-defined antigens (e.g. anti-streptolysin, anti-DNA, or anti-IgG(13)). The first systematic studies covering a broad spectrum of potential antigens used serological identification of antigens by expression cloning (SEREX), which allows for the systematic screening of putative antibody–antigen interactions, even if neither the antigen nor the antibody are known.(16) cDNA libraries derived from human testis, lung, and breast cancer, bovine and porcine muscle, and wheat germ were expressed in Escherichia coli and investigated by SEREX for reactivity with paraproteins from the sera of 114 patients with MGUS or MM. More than 6 × 108 paraprotein–antigen interactions were probed, resulting in the identification of only four antigens, each recognized by the paraprotein of only one patient.(17,18) In a complementary approach using a human fetal brain-derived macroarray and IgA or IgG paraprotein-containing sera, the paraproteins of 29 (15.1%) consecutive MGUS and MM patients reacted with paratarg-7 (P-7).(19) Paratarg-7 is identical to STOML2 (stomatin [EPB72]-like), also known as HSPC108 or stomatin-like protein and SLP-2,(20) that has also been reported to be expressed in all human tissues and overexpressed(21,22) in several cancers.(23) Other investigators have reported that P-7 modulates T cell activation,(24) and in a recent publication it was claimed that SLP-2 is required for stress-induced mitochondrial hyperfusion.(25) In an extension of our earlier study, the high frequency of P-7-specific paraproteins in the sera of MGUS/MM patients (35/252; 14%) was confirmed in a subsequent study.(26) Moreover, it was shown that all patients with P-7-specific paraproteins were carriers of a hyperphosphorylated version of the protein (pP-7) and that this hyperphosphorylation is inherited in a dominant fashion.(26,27) As only 2% of healthy Germans are carriers of pP-7, the pP-7 carrier state is associated with an increased risk (odds ratio, 7.9) to develop MGUS/MM. Thus, pP-7 is the first molecularly defined inherited risk factor known for any hematological neoplasm. Because of the autosomal-dominant inheritance of pP-7, it is of interest to determine the prevalence of the pP-7 carrier state and the frequency of pP-7-specific paraproteins in other ethnic groups. As the incidence of MGUS and MM is lower in Asians than in Europeans,(6,7) it was the aim of this study to compare a German population with a Japanese population with respect to the prevalence of the pP-7 carrier state and the incidence of P-7-specific paraproteins in MGUS and MM.