BV-2 microglia were activated by SARS-CoV-2 spike S1 protein, resulting in the production of pro-infammatory mediators TNFα, IL-6, IL-1β, and NO through activation of NF-κB and p38 MAPK, possibly as a result of TLR4 activation.[41] Moreover, the microglial hyperactivation in the brainstem, and in the hippocampus of COVID-19 patients with delirium, appears as a specific topographical phenomenon, and probably represents the neuropathological basis of the “COVID-19 encephalopathic syndrome” in the elderly.[47] Some studies have also been done on the mechanism of microglia activation in COVID-19. Here, NFKB1 is linked to COVID-19.