The proximity of TRIM67 to other genes linked to Alzheimer’s disease and schizophrenia (DISC1; Beecham et al., 2009; Carless et al., 2011), Parkinson’s disease (SIPA1L2; Nalls et al., 2014), and cognitive function (DISC2, C1orf131, GALNT2; Xu et al., 2017) by genome-wide association studies (GWAS), and the behavioral deficits revealed here associated with deletion of murine Trim67 are intriguing, potentially suggesting possible involvement of TRIM67 in human disorders or behaviors. This evidence concerns the gene FSAF1 and early-onset autosomal dominant Alzheimer disease.