Ciprofloxacin’s inhibition of CYP1A2 has been described as ‘relatively inconsequential’ [35] and the US Food and Drug Administration (FDA)’s Adverse Event Reporting System (AERS) supports the notion of several causes of fluoroquinolone-associated TdP, usually in the context of co-administration with another QT-prolonging drugs, underlying cardiac disease, renal impairment and electrolyte anomaly. This evidence concerns the gene CYP1A2 and heart disorder.