Experiments defining TREM2 function after CNS pathology have shown that blockade of TREM2 in animal models of multiple sclerosis leads to disease exacerbation by increasing leukocyte infiltration and demyelination [42], while intravenous application of TREM2-transduced myeloid cells facilitated repair by reducing axonal damage [43]. The gene discussed is TREM2; the disease is multiple sclerosis.