A compelling description of potential heteromerization mechanisms between CB1 and AT1 receptors accompanying reduced fibrosis in mouse liver (Rozenfeld et al. 2011) led us to hypothesize that CB1 receptor blockade would disrupt the Ang II‐dependent hypertension in (mRen2)27 rats, and results from our current study are congruent with this hypothesis. The gene discussed is AGT; the disease is hypertensive disorder.