LSECs become capillarized45 and their phenotype is transformed into a pro-inflammatory pattern, with the formation of the basement membrane, a significant reduction of fenestrae, and increased expression of pro-inflammatory mediators such as tumor necrosis factor α (TNF-α), macrophage inflammatory protein 1 alpha (MIP-1α), monocyte chemoattractant protein-1 (MCP-1), and chemokine (C-C motif) ligand 5 (CCL5).46 At the same time, LSECs recruit immune cells and activate HSCs and Kupffer cells to induce liver inflammation.47 (Figure 1(d)). The gene discussed is CCL5; the disease is Hepatitis.