Although previously reported data (29, 30) suggest that it may be explained, at least in part, by differences among CTD cohorts in terms of autoantibody concentration and specificity [high levels of anti-Ro/SSA-52kD are particularly frequent in SS, much less in SLE and rarely in SSc (159)], or disease-related inflammatory burden (and thus cytokine levels), the above electrophysiological data, by indicating that anti-Ro/SSA inhibit both calcium and hERG-potassium currents, provide a further pathophysiological mechanism possibly contributing to differences observed. Here, TRIM21 is linked to systemic sclerosis.