Ciprofloxacin’s inhibition of CYP1A2 has been described as ‘relatively inconsequential’ [45], and the US Food and Drug Administration (FDA)’s Adverse Event Reporting System (AERS) supports the notion of multifactorial causes of fluoroquinolone-associated TdP, usually occurring in the context of co-administration with another QT-prolonging drug, underlying cardiac disease, renal impairment and electrolyte anomaly. This evidence concerns the gene CYP1A2 and heart disorder.