Interestingly, in the carbon tetrachloride (CCl4)-induced fibrosis animal experimental model, it was observed that this cytokine secretion was stimulated by the upregulation of TNF-like ligand 1 A (TLA1A), both TNF-α and IL-1β, and also PDGF-BB in BMDMs, which were responsible for enhancing activation and proliferation of primary HSCs [112]. This evidence concerns the gene TNF and fibrosis.