MYD88 and myeloid sarcoma: The most recent elucidation of the mechanistic role of NETs in MS pathogenesis was performed by Wilson et al., showing that histones can directly activate T cells for T-helper 17 (Th17) differentiation via TLR2 and myeloid differentiation primary response 88 (MyD88), leading to the phosphorylation of signal transducer and activator of transcription (STAT3) [95], essential for Th17 cell responses [96].