Notably, all of these tissues showed histological evidence of severe lung parenchymal injury manifested as diffuse alveolar damage (exudative and early proliferative phases) with or without bronchopneumonia and/or microthrombi with no meaningful link between histological severity and ACE intensity, particularly in low and moderate ACE staining cases (Supplementary Fig. S1). This evidence concerns the gene ACE and bronchopneumonia.