Genetic deficiency of C1Q is a strong risk factor for development of SLE (systemic lupus erythematosus), triggering pro-inflammatory mediators, such as C5a and C3, and impaired cytokine production resulting in persistent and recurrent viral infections, known to be an exacerbating factor for SLE [28–31], but much less is known about the role of complement in SSc. Here, C3 is linked to systemic lupus erythematosus.