Several studies have shown that the PPARγ agonists, such 15d-PGJ2, ciglitazone, and pioglitazone, confer protection in neuroinflammatory and sepsis animal models through the inhibition of STAT, AP-1, and NF-κB activity as well as reduced Th1 differentiation [53–55]. This evidence concerns the gene SOAT1 and Sepsis.