TGFB1 and systemic sclerosis: Excessive phosphorylation of a signal transducer and activator of transcription 3 (STAT3) has been implicated as a driver of aberrant fibroblast activation.[26] STAT3 is a cytoplasmic transcription factor with important role in cell proliferation, migration, differentiation, and survival.[27] TGF‐β signaling triggers phosphorylation of JAK2, which then interacts with and phosphorylates STAT3 to induce a fibrotic response.[28] STAT3 signaling is hyperactivated in systemic sclerosis in a TGF‐β‐dependent manner, suggesting that STAT3 may be a core mediator of fibrosis.