Although TGFβ is widely regarded as an important driver of SSc pathophysiology [1], e.g., because it stimulates the excessive production of collagen type I by skin fibroblasts and enhances the contractile properties of these cells [10], its plasma and serum levels have been a controversial topic for many years; studies have reported increased [11–13], equal, and, similarly to our study, decreased levels [14, 15] of TGFβ in serum and plasma of the SSc patients. Here, TGFB1 is linked to systemic sclerosis.