In the development of diabetic retinopathy, overexpressed histone HIST1H1C/H1.2, an important variant of the linker histone H1, upregulates SIRT1 and HDAC1 to maintain the deacetylation of H4K16, leads to ATG proteins expression, and then promotes autophagy, inflammation and cell toxicity.93 Small-chain fatty acids treatment-reduced HDAC2 upregulates H3K27ac on ULK1 promoter, reduces ULK1 expression and autophagy flux and thus alleviate diabetic renal fibrosis94 (Fig. 3). The gene discussed is ULK1; the disease is diabetic retinopathy.