Many of such virus-induced factors have been reported as key factors in tissue fibrosis: GREM1 was recognized as a key pro-fibrotic factor in renal, pancreatic, and pulmonary fibrosis [55,56,57]; INHBE, a member of the TGFβ superfamily of proteins, was reported to be associated with dermal fibrosis [58]; IL-4 is even more active than TGFβ in inducing collagen synthesis in human skin fibroblasts [59,60], and can drive fibroblast differentiation and promote pro-fibrotic macrophages activation [61]. Here, INHBE is linked to pulmonary fibrosis.