Type I IFNs induce the expression of Schlafen genes.[23] SLFN12 has been shown to be downregulated during T-cell activation in primary human cells.[24] From clinical observations and genetic studies,[4,6,25–27] there is convincing evidence that MS pathology is driven by T-cells, and IFN beta type I is an approved therapy for MS, making SLFN12 a biologically plausible gene of interest for MS. Here, SLFN12 is linked to myeloid sarcoma.