This issue does not stem from the models, which show high accuracy on current data, but rather are representative of a pattern of widespread susceptibility seen consistently across experimental infections (65.2% of mammals susceptible, CI: 42.7–83.6%), our wider training data (82.2%, CI: 72.7–89.5%), and predictions from both the ACE2-based ensemble and host phylogeny-based models (87.6% and 42.6%, respectively). This evidence concerns the gene ACE2 and infection.