Steatosis in hepatocytes enhances vulnerability to other damaging factors (31), which could promote the generation of reactive oxygen species (ROS), tumour necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), interleukin 1 (IL-1), and plasminogen activator inhibitor-1 (PAI-1) to further activate signalling pathways and increase susceptibility to genetic polymorphisms (32–35). This evidence concerns the gene IL6 and steatosis.