This is in agreement with our previous findings showing that IRF5 is a downstream target of CB1R in macrophages, in which it drives the CB1R-mediated increase in TNF-α secretion, and its in vivo knock-down in macrophages prevents the loss of pancreatic islet β-cells and the development of type 2 diabetes [42]. Here, IRF5 is linked to type 2 diabetes mellitus.