CDKN2A and myeloid sarcoma: Finally, chronic inflammation may influence biological ageing in MS.34 Whereas chronological age is fixed, aspects of biological ageing are reversible, offering a pathway to restore remyelination capacity in preclinical models.5,7 There are an increased number of SOX2+ progenitor cells expressing p16Ink4a—a marker of cellular senescence—in white matter lesions of progressive MS patients compared to age-matched controls.35 This senescence phenotype in SOX2+ progenitor cells appears to suppress the maturation and thus myelinating capacity of OPCs in vitro.