By screening for 33 polymorphisms in the human ERAP1 gene, Yamamoto et al. identified the association of ERAP1 variant rs30187 (K528R) with essential hypertension and hypothesized that the R528 form of ERAP1 was less active than the K528 form, leading to hypertension due to reduced bradykinin formation and/or lower inactivation of angiotensin II (Figure 1d) [43]. The gene discussed is AGT; the disease is hypertensive disorder.