In detail, through a human-like mice model of RA with transgenic activation of the TNF-α pathway, it has been shown that an increased level of TNF-α in RA could augment Ox-LDL uptake and activate the LOX-1/NFκB/Arg2 pathway, which reduced bioavailability of NO and levels of cGMP [160], hence leading to endothelial dysfunction. The gene discussed is TNF; the disease is endothelial dysfunction.