Moreover, investigating the effects of NO2-OA on Mlp−/− cardiomyocytes could elucidate an additive effect of NO2-OA in the failing heart beyond attenuated CF activation, especially as beneficial properties of NO2-OA on ischemic heart failure in vivo and on malignant arrhythmias in isolated cardiomyocytes were previously shown [19,50]. The gene discussed is CFTR; the disease is cancer.