The present-day understanding of PPARs primarily indicates the anti-inflammatory potential of this receptor, which exerts its anti-inflammatory effect through the inhibition of NF-κB. At the same time, TLR signaling pathways activate NF-κB. The crosstalk between PPARs, TLRs, and NF-κB is of great importance in the pathogenesis of the inflammatory process in asthma. This evidence concerns the gene NFKB1 and asthma.