For example, release of astrocyte-derived TIMP-1 in an experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis has a protective effect and results in myelin sparing (Crocker et al., 2006) and attenuates the effect of IL-1β on the wound healing responses in vitro (Johnson and Crocker, 2015). This evidence concerns the gene IL1B and multiple sclerosis.