Finally, Walkey et al3 also highlight the potential of upstream therapy to tackle sepsis-associated new-onset AF. Sepsis triggers an inflammatory response, and this may directly increase the risk of AF via increased catecholamine release. Previous work has demonstrated the significant rise in C-reactive protein level prior to the onset of sepsis-induced AF.2 Thus, potential suppression of overwhelming inflammation may have a role in reducing the incidence of, or even preventing, subsequent arrhythmia. For example, the potential of perioperative use of corticosteroids in cardiac surgery to prevent AF has been promising.11 In sepsis, systemic steroids, however, may be counterproductive, so other options need to be found. Given the high prevalence of AF, the challenge is to accurately identify those patients who have an increased propensity for developing AF and those at particular risk of complications. Indeed, sepsis may simply be the catalyst to expose the vulnerability of developing this arrhythmia (and its complications).