Moreover, inhibition of RUNX1 has been shown to enhance symptoms of lung fibrosis in a mouse model (O’Hare et al., 2021), while overexpression of RUNX1 has been observed in the lungs of severe COVID-19 patients who died of the disease, with widespread thrombosis and microangiopathy and related vascular angiogenesis much more prevalent in COVID-19 than in influenza (Ackermann et al., 2020). This evidence concerns the gene RUNX1 and pulmonary fibrosis.