FGA and systemic sclerosis: APOB is involved in platelet activation [30]; C9 is a component of the membrane attack system of the complement system, which has already been implicated in SSc pathogenesis [31]; Gal‐3 is involved in fibrogenesis via macrophage recruitment, TGF‐β production, and fibroblast proliferation [32]; FGA, ORM, and HP are acute‐phase proteins, whose concentrations increase in response to inflammation and participate in the initiation of tissue remodeling following injury [33, 34, 35, 36].