Studies have shown that oral treatment of patients with ERY followed by its metabolism by cytochrome P450 3A (CYP3A) leads to an increase of the drug concentration in the blood plasma, consequently leading to the development of cardiac arrhythmia and torsade de pointes (TdP) by blocking human-ether-a-go-go gene (hERG) and prolonging QTc intervals [7]. Here, KCNH2 is linked to torsades de pointes.