TGFBR3 and systemic sclerosis: Taken together, these results propose a scenario in which SSc fibroblasts present different basal characteristics when compared to normal fibroblasts and, among them, SSc fibroblasts express higher Betaglycan levels (6), thus causing an excessive response to TGFβ stimulation and a consequent overproduction of pro-fibrotic proteins (6, 48).