More recently, Laroni et al. added new data on the functioning of the NK subset by identifying a CD56brightCD16− NK cells subset that was able, upon inflammatory cues, to kill autologous CD4+ T cell proliferation via granzyme B release and NKp30 and NKp46 involvement [174], thus reinforcing the notion that this subset of NK cells could be associated with the regulation and control of MS. This evidence concerns the gene CD4 and myeloid sarcoma.