Expression of miR‐181b‐5p was implicated in a number of important cellular processes, including attenuation of pro‐inflammatory NFκB signaling in endothelial cells, suppression of myeloid differentiation in acute myeloid leukemia, and mediation of hypoxia‐driven angiogenesis.[36] In the present study, delivery of miR‐181b‐5p was imperative in lowering glucose uptake, shifting metabolic function toward lowered glycolytic activity, and reducing mtROS production in macrophages. The gene discussed is NFKB1; the disease is acute myeloid leukemia.