For instance, we found that PPARα KO increased the expression of Il12rb1 (Interleukin-12 receptor beta 1) by 48 h post-stroke; signaling through IL12Rβ1 promotes interferon-gamma (IFNγ) production [40], which worsens neuroinflammation post-stroke by activating immune cells to produce more inflammatory cytokines and chemokines. This evidence concerns the gene IFNG and stroke disorder.