We observe considerably increased performance in the identification of pathogenic missense mutations from AR genes compared to AD genes as measured by ROC AUC (0.71 vs. 0.67 for full | ΔΔG | , AR and AD respectively), which is even greater when the homozygous set of putatively benign AR gnomAD variants are used (0.77; Fig. 2c). This evidence concerns the gene AR and Alzheimer disease.