On the basis of our previous observations of elevated serum levels of BAFF in patients with anti-Jo-1 antibodies [13] and the demonstration of IFN-α-inducing capacity of anti-Jo-1 or anti-Ro52/anti-Ro60-positive sera [23], we postulate that the BAFF pathway could be of particular relevance for a subset of myositis patients with autoantibodies. This evidence concerns the gene TRIM21 and myositis disease.