CXCL8 and steatosis: In their model, although high palmitic acid concentrations induced high toxicity and tissue damage, as well as several markers of the inflammatory (e.g., IL-8) and pro-fibrotic process (e.g., TIMP-1, PDGFRβ, collagen I and III), palmitic acid did not induce lipid accumulation or a steatosis-like phenotype.