STAT3 and atherosclerosis: Furthermore, MIAT greatly enhances signal transducer and activator of transcription 3 (STAT3) expression by acting as a molecular sponge to sequester miR-181b, promoting the development and progression of atherosclerosis via the miR-181b/STAT3 regulatory pathway, however, this effect is counteracted by miR-181b (52) overexpression.