In addition to angiogenesis, both inflammatory mediators (IL-1β, IL-6, IL-8, TNF-α and so on) and immune cells (neutrophils, macrophages, dendritic cells, NK cells, T cell subsets and so on) crucially contribute to the formation and progression of EMs, although whether inflammation is the cause or the result of EMs is uncertain [39]. The gene discussed is IL1B; the disease is eosinophilia-myalgia syndrome.