It has previously been shown that resident cardiac macrophages can respond to hypertension by activation of pro‐inflammatory signalling,30 due to exposure to altered mechanical forces.31 Additionally, DS‐induced activation of mineralocorticoid receptors could also trigger cardiac inflammation and fibrosis, independent of hypertension,32, 33 implying that multiple mechanisms could orchestrate the observed response in the hypertensive rats. The gene discussed is NR3C2; the disease is hypertensive disorder.