CDKN2A and premenstrual tension: These include decreased telomere length in peripheral leukocytes,8–10 increased DNA and mitochondrial damage in neurons in situ,11–13 increased epigenetic age in glial cells,14 a senescence-associated secretory phenotype (SASP) in microglia and astrocytes,15,16 and p16Ink4a/CDKN2A expression in glia, including neural stem/progenitor cells (NSCs) and astrocytes.16–18 The increasing evidence linking PMS to senescence underscores the need for investigation into how the accumulation of senescent glial cells contributes to disease pathogenesis and persistent smoldering inflammation.