Furthermore, deletion of CCAAT/enhancer binding protein homologous protein promoted the expression of suppressor of cytokine signaling 1 and 3, which then inhibited signal transducer and activator of transcription 6/peroxisome proliferator-activated receptor gamma (STAT6/PPAR-γ) signaling, thereby attenuating the induction of M2 macrophages and alleviating idiopathic pulmonary fibrosis [37]. Here, DDIT3 is linked to pulmonary fibrosis.