Whilst it is important to acknowledge these limitations, the strengths of the present study are that it: (i) highlights the potential for all the drugs studied here to interact with hERG; (ii) provides specific observations that can form the basis for experimental hypothesis formation and testing; and consequently (iii) provides a valuable basis from which future experimental investigation of both hERG inhibition and overall cardiac arrhythmia liability can be tested. The gene discussed is KCNH2; the disease is cardiac arrhythmia.