Moreover, a recent work combining Nod1 and Nod2 deficiency under the Ldlr−/− background shows similar results to those reported in this work [28]; however, in our animal model, whereas NOD1 was highly upregulated under HFD regime, NOD2 levels remained unchanged (Figure S9) stressing the relevance of NOD1 in the context of atherosclerosis. The gene discussed is NOD2; the disease is atherosclerosis.