The etiology of calcinosis remains uncertain, with proposed mechanisms including microvascular changes [3,4,5], the dysregulation of components of the innate immune system [6], and associations with specific autoantibodies (e.g., anti-MDA5, anti-NXP2, anti-PM/Scl, anti-centromere, and anti-topoisomerase I) [7]. The gene discussed is PRB1; the disease is calcinosis.