Noteworthily, these results were not seen in TLR3 KO or Kupffer cell-depleted mice, which suggest that TLR3 activation in Kupffer cells leads to an elevated IL-1β expression, thus driving IL-17A secretion by γδ T cells early during alcohol-associated liver disease and increased CD4+ T-cell secretion of IL-17A during the end stage of alcohol-associated liver disease (74). This evidence concerns the gene CD4 and liver disorder.