reduced endothelial cell death induced by DOXprevented the oxidative stress and ROS formed by DOX inductionabrogated the effect of DOX on the induction of the expression of ICAM‐1 and VCAM‐1 as well as the adhesion of monocytesrestored nitric oxide (NO)‐levels and eNOS expression decreased by DOXsoothed the activation of inflammatory responses such as NFκB and cytokines in HUVECs and in vivoprevented the cardiac hypertrophy and expression of eNOS, iNOS and 3‐Nitrotyrosine in tissues of the aortaaverted cytotoxicity created by DOX in non‐cancerous tissues. The gene discussed is NFKB1; the disease is cardiac hypertrophy.