Moreover, a high-fat diet could promote the resistance of lung fibroblasts to apoptosis by inhibiting the expression of the death receptor Fas (also called CD95), leading to the progression of pulmonary fibrosis.251 The Fas promoter in fibroblasts from the murine model of pulmonary fibrosis displayed a reduction in histone acetylation and an increase in H3K9me3, which correlated with elevated expression of HDAC2 and HDAC4.252 A high-fat diet has also been shown to induce H4K16ac accumulation, leading to pro-fibrotic gene overexpression and collagen deposition in lung fibroblasts.253,254. The gene discussed is HDAC2; the disease is pulmonary fibrosis.