These authors showed that the inhibition of CYP1B1 significantly attenuates isoprenol-induced cardiac hypertrophy, with protection afforded by the modulation of superoxide anion, MAPKs, and nuclear factor-κB (NF-κB) [20], whilst the overexpression of CYP1B1 significantly induces cellular hypertrophy and mid-chain HETE metabolites. Here, NFKB1 is linked to cardiac hypertrophy.