The expression of miR-34a in adipose tissues was progressively increased with the development of dietary obesity and was related to obesity-induced glucose intolerance, insulin resistance, and systemic inflammation, as well as a shift in polarization of adipose-resident macrophages from M1 to M2 phenotype via inhibition of Krüppel-like factor 4 (Klf4) expression [121]. The gene discussed is KLF4; the disease is Glucose intolerance.