This means that dystrophin deletion, along with other off-target gene deletions, is also present as a second hit in this model; the authors indeed note a decrease in dystrophin RNA levels but theorize that it was a secondary effect of cardiomyopathy, then find that a dual deletion of the MR prevented many of the heart phenotypes in GR-null mice (Oakley et al., 2019). The gene discussed is NR3C1; the disease is cardiomyopathy.