Ondansetron can block this channel, resulting in lengthening of the repolarisation.[6] Drugs like granisetron and dolasetron act on the Na+  and K+  channels to prolong QRS or QT interval, resulting in ventricular arrhythmias.[6] The sub-micromolar   affinity of ondansetron for K+  channels is possibly responsible for the prolongation of cardiac repolarisation, thus resulting in conduction disturbances.[6] Secondly, the cardiovascular effects of serotonin are mediated by 5HT1 , 5HT2 , 5HT3 , 5HT4  receptors, which are distributed throughout the cardio vascular system. The gene discussed is HTR2A; the disease is Ventricular arrhythmia.