As previously reported, elevated GLUL mRNA level and local GLUL immunoreactivity are linked to macrophage M1-M2 phenotype and are associated with fibrous cap thinning, thus plaque destabilization [47]; moreover, macrophage deficiency in GLS1 to reduce macrophage glutaminolysis was seen to exacerbate atherosclerosis [8]. This evidence concerns the gene GLS and atherosclerosis.