We observed sex‐specific enrichment for a number of immune‐, inflammatory‐, damage‐related, and stress‐response pathways, including hypoxia, DNA repair, OXPHOS, and UV response, all of which are related to well‐known AD risk factors,75 with some enriched in opposite directions across sexes, such as TNF‐α signaling via NF‐κB, MYC targets, and OXPHOS pathways. The gene discussed is NFKB1; the disease is Alzheimer disease.