In light of recent reports showing that eliminating or rejuvenating senescent microglia may represent alternative treatment strategies for neurodegenerative diseases [49,50,53], it is reasonable to speculate that interventions intended to halt or delay microglial senescence (such as the transgenic p16-InkAttac mice and senolytic drugs) might lead to actual reductions in the incidence of delirium (not just in elderly individuals) as well as delirium-related neurocognitive sequelae. The gene discussed is CDKN2A; the disease is delirium.