2011; Kawano et al. 2012), an alternative, but not exclusive, explanation could be that clonidine, through its inhibitory action on RSNA, decreases the release of renin and the ensuing formation of angiotensin II, which have been shown to be strongly increased during sepsis (Schaller et al. 1985; Doerschug et al. 2010). As a consequence, vasoconstrictor responses to angiotensin II would be enhanced. Unfortunately, in this study, plasma renin activity or angiotensin II concentrations were not measured (Lankadeva et al. 2015). The gene discussed is REN; the disease is Sepsis.