“…For example, MAPK activation can regulate the expression of proinflammatory cytokines, including IL-1, IL-6, and TNF- α , as well as cyclooxygenase-2 (COX2) and inducible nitric oxide synthase (iNOS) [ 24 ]. The onset of DEACMP is closely related to many immune cells and inflammatory factors, such that the infiltration of T cells, B cells, macrophages, and neutrophils and the cascade-like release of inflammatory factors such as interferon- γ , interferon- α , IL-6, IL-8, and others participate in the occurrence of DEACMP [ 8 ]. Thus, it is plausible that alterations in cadherin function through genetic variation results in changes in ROCK and MAPK signaling that impact the repair of demyelination damage and inflammatory responses during DEACMP pathogenesis.…”