Kidney ischaemia is associated with a loss of intracellular potassium and an increase in intracellular levels of sodium, chloride and calcium; however, the mechanisms involved in the loss of cellular ion homeostasis are unknown. A new study has revealed a critical role for the nonselective cation channel TRPM2 in promoting acute kidney injury (AKI) via a mechanism that involves the activation of RAC1, oxidative stress and mitochondrial apoptotic pathways. The researchers believe that targeting TRPM2 or RAC1 might be a strategy to reduce or prevent ischaemic AKI.