This idea is supported by a paper, showing that the administration of an iNOS selective inhibitor L-N6-(1-iminoethyl)-lysine accelerated the progression of vasculopathy in transplantation atherosclerosis, and transduction with iNOS using an adenoviral vector has been shown to completely suppress the development of allograft arteriosclerosis (Forbes et al., 2013[15]; Shears et al., 1997[37]). Here, NOS2 is linked to arteriosclerosis.