Damiani S, Fiorentino M, De Palma A, et al. - The lung tissues of nine patients who died of SARS‐CoV‐2‐associated disease were examined at the autopsy to describe the disease associated lung pathological and immunohistochemical postmortem findings. Histological changes consistent with diffuse alveolar damage were noted in various evolution phases ranging from acute exudative to acute proliferative to fibrotic phase. In most cases not related to sources of embolism, alveolar damage was linked with marked involvement of the vascular component in both the interstitial capillaries and the mid‐size vessels, with capillary fibrin micro‐thrombi, as well as organized thrombi even in medium‐sized arteries. In addition, there was eosinophilic infiltrate, probably reactive to pharmacological treatment. The lung tissues of all the nine patients had isolation of the viral RNA of SARS‐CoV‐2. Immunohistochemistry for the receptor of the SARS‐CoV‐2, ACE2, and its priming activator TMPRSS2 revealed co‐localization of both proteins in airway cells. In the areas of histological diffuse alveolar damage (DAD), both endothelial cells and alveolar type I and II pneumocytes, in particular, expressed the ACE2 protein. Pneumocytes, but not endothelial cells, expressed TMPRSS2 in addition. In the course of SARS‐CoV‐2 infection, the recognition of the cause of death is more likely multi‐factorial.