As expected, doxorubicin induced mitochondrial dysfunction, activation of NF-κB, and upregulation of proinflammatory cytokines (e.g., IL-6, IL-1β, and TNF-α) in HUVECs, triggering EndMT, a crucial process in the initiation and progression of atherosclerosis. The gene discussed is NFKB1; the disease is atherosclerosis.