TLR4 and autoimmune myocarditis: For instance, in experimental autoimmune myocarditis, HMGB1 facilitated macrophage reprogramming towards a pro-inflammatory M1 phenotype via TLR4-PI3Kγ-Erk1/2 pathway, as demonstrated by a reduction in infiltrating M1 macrophages following HMGB1 stimulus and TLR4 blockade, PI3Kγ inhibition, or Erk1/2 inhibition [84].