It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28].