ALP has been shown to reduce both the formation of uric acid and the production of oxidative free radicals41 by restoring Nrf2 and HO‐1 expressions,42 and enhancement of Nrf2 has recently been shown to be a mechanism by which treatments attenuate DCM.43, 44 We thus postulated that enhancement of Nrf2 may be a major mechanism whereby ALP attenuates DCM. The gene discussed is HMOX1; the disease is familial dilated cardiomyopathy.