KCa3.1 silencing leads to alterations in key nuclear factors, including downregulation of cfos and NR4A1 and upregulation of PPARα, PPARγ, and PGC1α (1.8-fold, p < 0.05) subsequently predicted to lead to inhibition of key atherogenic processes including leukocyte infiltration, macrophage activation, SMC proliferation, and necrosis, resulting in inhibition of atherosclerosis observed in the current experiment. The gene discussed is PPARG; the disease is atherosclerosis.