Altogether, the current balance of evidence suggests that variants on the BIN1 locus behave like APOE-ε4: pathogenic BIN1 variants increase the overall risk of LB pathology simply by increasing the risk of AD pathology (which is frequently accompanied by LB pathology), but they do not affect the risk of AD–LB+ pathology or the risk of co-pathology (AD+LB+) among AD+ individuals. Here, BIN1 is linked to Alzheimer disease.