Other researchers that focused on cytokine roles in neuroinflammation suggest that IL-33 may at least in part be responsible for inducing a transition from the Th1 to the Th2 immune response and for inhibiting the Th17 immune response, which can act as an anti-inflammatory and lessen cognitive impairment following CNS damage, such as in severe cases of COVID-19 [7,35]. This evidence concerns the gene IL33 and COVID-19.