As a consequence of the CNVs in this region, genotyping data across LRRC37A and LRRC37A2 is of low confidence and quality, and as such is excluded from GWAS analyses, as is visible in any association plot, and likely explains why the peak genetic signal for PD association was close to MAPT and KANSL1. The association between LRRC37A/2 variants and any disease or phenotype has therefore never been tested, and it is likely that additional variation within LRRC37A/2 itself is contributing to its altered expression and function that may also impact PD risk. This evidence concerns the gene KANSL1 and Parkinson disease.