Sporadic inclusion body myositis (sIBM) is diagnosed by its clinical and pathological features. sIBM is clinically characterized by asymmetric weakness of finger flexors with slow progression and resistance to immunosuppressive therapy. Pathologically, sIBM shows an inflammatory feature, namely T-lymphocyte infiltration into endomysium, and degenerative features, by presence of rimmed vacuoles (RV) and aggregated proteins like amyloid, p62, TDP-43 and others in myofibers. Although sIBM has been diagnosed clinically and pathologically, it is quite difficult to make a correct diagnosis for sIBM only by pathological evaluation without any clinical information, if pathological hallmarks such as RV and amyloid inclusions, are absent in muscle biopsy. Serological biomarkers for sIBM had not been found for a long time, however recently the autoantibody to cytosolic 5′-nucleotidase 1A (cN1A) was reported as a highly specific marker to sIBM. In this study, we tested the diagnostic utility of this anti-cN1A autoantibody in plasma of sIBM patients. We measured a titer of anti-cN1A autoantibody by ELISA in plasma samples of 315 patients who were suspected to have inflammatory myopathy. Among them, the antibody was positive in 12 of 34 sIBM patients, 5 of 18 polymyositis, 0 of 22 dermatomyositis, 7 of 37 SRP myopathy, and 9 of 204 others (total 33 of 315). Anti-cN1A autoantibody found out more than one-third of sIBM patients as previously reported but also found polymyositis (28%) and SRP myopathy (19%). The presence of anti-cN1A autoantibody in some patients with polymyositis may raise a possibility that those patients may in fact have had sIBM. In fact, previous studies also reported similar results. However, increased titer in SRP myopathy has never been reported. Considering that SRP myopathy has markedly different clinical and pathological features from sIBM, SRP myopathy may have a different mechanism to produce anti-cN1A autoantibody although further studies are necessary.