Further, use of RIPK1-inhibitor Nec-1s or genetic deletion of RIPK3/MLKL could ameliorate TNF/TNFR1-induced neuronal and oligodendrocyte death in MS models, suggesting a functional link between necroptosis and neurodegeneration in MS-like pathology, and thus, necroptosis signaling holds great promise for therapeutic intervention. This evidence concerns the gene RIPK3 and myeloid sarcoma.