Indeed, it has been reported that EndMT contributes to endothelial dysfunction during inflammatory conditions, and that some inflammatory mediators, such as IL-1β, TNF-α, nuclear factor kappa B (NF-κB) transcription factor, and endotoxins, can activate ECs and convert them to mesenchymal-like cells through the EndMT process (6, 7, 31). The gene discussed is IL1B; the disease is endothelial dysfunction.