This inconsistency is due to different tissues (lungs, liver, kidneys, or skin), cell types (macrophages vs. fibroblasts), pathologic stages of fibrotic diseases (inflammatory stage vs. fibrosis stage), and various types of G-protein signaling triggered by CB1R. Previous studies have paid close attention to inflammation period and macrophage functions in pulmonary fibrosis, and the inhibition of CB1R exhibited anti-inflammatory properties (Cinar et al., 2017). Here, CNR1 is linked to pulmonary fibrosis.