Western blot results showed that ectopic expression of miR-26a led to a significant reduction of the protein levels of p-p65 and p-IκBα but had no obvious effect on the protein levels of p65 and IκBα in ox-LDL-treated HAECs, suggesting that miR-26a overexpression significantly inhibited activation of the NF-κB pathway in atherosclerosis in vitro (Fig. 7a). The gene discussed is NFKB1; the disease is atherosclerosis.