This evidence, together with our results, points to defective regulatory functions in Bregs from patients with SSc, which could be partially explained by their inability to increase TIM-1 and IL-10, and probably other inhibitory molecules, upon stimulation, while expressing activation molecules and pro-inflammatory cytokines, such as IL-6 [25, 28], tipping the balance toward a more pro-inflammatory or pro-fibrotic profile. The gene discussed is IL6; the disease is systemic sclerosis.