Last, hypoxia in the lungs of severe COVID-19 patients can activate hypoxia-inducible factor-1α, which binds to Foxp3 and targets the proteasome for degradation [34], leading to the abrogation of Foxp3 autoregulatory transcriptional loop and thereby impeding the differentiation of Tregs [35]. This evidence concerns the gene FOXP3 and COVID-19.