Rapidly activating component of delayed rectifier potassium current (I(Kr)) 
plays a key role in the repolarization phase of cardiac action potential. Human 
ether-a-go-go-related gene (HERG) encodes the alpha subunit of this potassium 
channel. Mutations of HERG gene induce genetic long QT syndrome (LQTS). 
Furthermore, I(Kr)/HERG is the target of some drugs which may cause cardiac QT 
interval prolongation. Some other drugs with different chemical structures also 
may block the channel and prolong QT interval, which even developed into 
acquired arrhythmias. This review summarized the recent progress of structure, 
gating mechanisms and functions of I(Kr)/HERG channel, I(Kr)/HERG related 
arrhythmias, interaction between K+ channel and drugs, and strategies of 
grading-up the I(Kr)/HERG target.