Although theoretical models have demonstrated that GWAS findings can reflect the contributions of one or more uncommon or rare variants, empirical data reporting such synthetic associations remain sparse, especially for complex disorders.[30] The variant rs34166160, located in intron 1 of NINJ2, showed the strongest association with incident ischemic stroke, which was slightly attenuated after accounting for the effects of the GWAS sentinel SNP rs12425791, suggesting possible allelic heterogeneity at this locus. Here, NINJ2 is linked to ischemic stroke.