Another mechanism study found that miR-140-5p expression is significantly decreased in MS patients; signal transducer and activator of transcription 1 (STAT1) is a functional target of miR-140-5p, and overexpression of miR-140-5p suppresses phenomenological Th1 differentiation by inhibiting the activation of STAT1 and the expression of its downstream target, T-bet (Guan et al., 2016). Here, STAT1 is linked to myeloid sarcoma.