On the other hand, as the disease progresses to NASH, impaired LSEC autophagy enhances the expression of chemokines, cytokines, and adhesion molecules, such as C-C motif chemokine ligand 2 (CCL2), CCL5, interleukin-6 (IL-6), and vascular cell adhesion molecule 1 (VCAM-1), and promotes the development of liver inflammation, endothelial-to-mesenchymal transition, and liver fibrosis [14]. This evidence concerns the gene CCL2 and digestive system neoplasm.