CCL2 and COVID-19: Because there is no evidence of direct cytopathic virus damage, the latter appears to be associated with the marked inflammatory activation produced by the infection [20]; in fact, molecular analyses revealed that during severe COVID-19, genes frequently linked to hepatic stellate cells (HSCs) activation and liver fibrosis, such as interleukin 6 (IL6), interleukin 1 (IL1), tumor necrosis factor α (TNF-α), interleukin 10 (IL10), and interferon α (IFN-α), as well as vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein 1 (MCP-1), are overexpressed [21].