For instance, the overexpression of let-7 in VSMCs inhibits inflammatory responses including proliferation, migration, and monocyte adhesion through the regulation of PDGF and tumor necrosis factor (TNF)-α signaling pathways; the depletion of Lin-28 Homolog B, a negative regulator of miRlet-7, leads to the suppression of the TNF-α-induced upregulation of interleukin (IL)-6 and PDGFR in VSMCs; and the restoration of let-7 levels suppresses vascular inflammation mediators including IL-6, IL-1β, and NF-κB, thereby attenuating atherosclerosis as well as diabetes [52]. The gene discussed is PDGFRB; the disease is atherosclerosis.