Recently, we reported that cordycepin attenuated ER stress-triggered renal tubular injury in vitro and in vivo[13]. In the present report, we also show that cordycepin inhibited activation of NF-κB by TNF-α in renal tubular cells, suggesting that cordycepin is useful for the treatment of inflammatory kidney diseases. However, therapeutic utility of cordycepin on kidney diseases might have a ‘Janus face’. Although it is renoprotective in ER stress-related diseases, it could be renotoxic in some pathologies where TNF-α plays a critical role. For example, some reports have suggested that TNF-α was causative of renal tubular apoptosis in urinary tract obstruction and ischaemia–reperfusion injury [31],[32]. If so, in these pathological situations, treatment with cordycepin might exacerbate renal diseases via enhancement of apoptosis