TGF-beta induces the expression of EGFR ligands, which in turn activate EGFR. Of relevance, TGF-beta was one of several pro-inflammatory cytokines that were observed to be highly upregulated in SARS-CoV patients (120) (121) (122), and mouse models of SARS-CoV infection showed interferon, cytokine and lung-associated wound-healing and ARDS-related genes (123). These findings are consistent with TGF-beta being profibrotic, as has been demonstrated in animal models (124). The kinase inhibitor, sorafenib, attenuated bleomycin-induced pulmonary fibrosis in a preclinical model (125) and ameliorated fibrosis in liver fibrosis models through STAT3 inhibition and downregulation of TGF-beta- and PDGFRβ-mediated pathways of fibrogenesis (126).