The lack of T1D-related autoimmunity in our cohort of SARS-CoV-2 patients, which must obviously be confirmed in follow-up studies extended over a longer period of time, seems to be in contrast with the hypothesis that the dysregulation of ACE2 activity following COVID-19 infection could induce beta-cell damage and new onset diabetes [4], at least in the time window that we investigated, ranging from 1 to 11 months from the first SARS-CoV-2 positive oropharyngeal swab. The gene discussed is ACE2; the disease is Autoimmunity.