In conclusion, the authors suggested that the anti-infection effects of N-3 PUFAs are associated with the inactivation of the NF-κB signaling pathway and the reduced expression of angiotensin-converting enzyme 2 (ACE2) and downstream transmembrane serine protease 2 in human endothelial progenitor cells (hEPCs), following the stimulation of the bacterial metabolite trimethylamine-N-oxide (TMAO) [115]. The gene discussed is ACE2; the disease is infection.