ACE2 and thrombotic disease: While forced overexpression of ACE2 in OE and forebrain neurons (Foxg1Cre; LSL-hACE2+/0 and Baf53BCre; LSL-hACE2+/0 in Figs 9 and S16) is sufficient to cause rapidly lethal hypoxemic respiratory failure with intravascular thromboses (hallmarks of COVID-19 acute respiratory failure), forced expression of ACE2 in the entire lung epithelium only resulted in a mild, transient hypoxemia (ShhCre; LSL-hACE2+/0 in Fig 8), suggesting organ-specific responses to SARS-CoV-2 infection.