Recent work suggests that their beneficial role in infection control may inadvertently contribute to AD progression, and that neutrophil‐driven inflammation and immune regulation could represent novel therapeutic targets for AD.[40] The correlation between APOE alleles and this signature suggests that the role of e2 in modulating inflammatory response could be enacted in non‐e2 carriers by direct targeting of this signature. The gene discussed is APOE; the disease is Alzheimer disease.