Interestingly, several studies have correlated increased plaque deposition to increased Inpp5d expression in humans and animal models, therefore, suggesting that disease-related SNPs impair the functionality of SHIP-1 but not its expression, which may in turn enhance PI3K-AKT signaling to exacerbate microglial responses during the early stages of Alzheimer’s disease development [151, 154, 155]. This evidence concerns the gene INPP5D and early-onset autosomal dominant Alzheimer disease.