Recall-by-genotype of less common, missense single-nucleotide variants (for example, functional, amino-acid change conferring SNPs within genes such as ABI3, PLCG2, TREM2) could also further provide mechanistic insight into the aetiology of preclinical AD, with known functional roles in modifying immune system physiology [51, 52], which have further been linked to features of brain health [53–55]. The gene discussed is TREM2; the disease is Alzheimer disease.