SOAT1 and neoplasm: It is worth mentioning however, that while we cannot fully explain how garcinol induced hsa-miR-181d inhibited the activation of STAT3 and STAT5, our data finds some corroboration in increasingly documented role of miRs in the (de)activation of the JAK-STAT signaling [46,47,48], and of particular interest is miR-204 which similarly had very insignificant effect on total STAT3 expression, but impaired STAT3 phosphorylation, consequently inducing cancerous cell apoptosis and suppressed cell proliferation, migration in vitro and tumor growth in vivo [48,49].