Studies investigating the composition of human MS lesions have shown that microglia in active MS lesions exhibit a rather activated phenotype with an upregulation of activation markers such as human leukocyte antigen (HLA)-DR, which is nearly absent in microglia under homeostatic conditions [97], and the concomitant downregulation of homeostatic marker proteins, such as the purinergic receptor P2Y (P2RY12), transmembrane protein 119 (TMEM119) and the fraktaline receptor CX3C chemokine receptor 1 (CX3CR1) [98]. This evidence concerns the gene CX3CR1 and myeloid sarcoma.