Similarly, the polarization state of macrophages plays a pivotal role in the development of chronic inflammation, further modulating the immune response within lesions through the secretion of various cytokines and chemokines.[60] Additionally, the activation of TLR1/2 and NLRP3 pathways, as upstream events in this process, may directly contribute to the persistence and exacerbation of chronic inflammation in EMs lesions.[61] Future research targeting these pathways and cellular processes is expected to provide novel strategies and targets for the treatment of EMs. This evidence concerns the gene TLR1 and eosinophilia-myalgia syndrome.