Specifically, in regard to p-tau as a result of long COVID or COVID-19, we wanted to highlight the findings that increased calcium/cAMP/PKA and CaMKII activity, RyR (Ryanodine receptor) leakage, and dysregulated intracellular calcium levels in general are reported along with altered glutathione disulfide (GSSG)/glutathione (GSH), and importantly, this downstream has been implicated to be the causation of the observed hyper-p-tau in COVID-19 brains compared to controls. The gene discussed is CAMK2G; the disease is COVID-19.