FOXP3 and COVID-19: Central to this, dysfunction is primarily driven by the COVID-19-associated cytokine storm, in which elevated IL-6 and TNF-α destabilize Tregs through epigenetic reprogramming—specifically, through STAT3-dependent deposition of repressive H3K27me3 marks at Foxp3 enhancers and synergistic suppression of maintenance signals mediated by NF-κB and PKCθ.