Based on these observations, the authors concluded that tubular epithelial damage represents a separate pathophysiological mechanism that importantly contributes to Stx2-mediated acute kidney failure, most likely due to electrolyte disturbance (Porubsky et al., 2014), which also occurred in our mice treated with EHEC O157 OMVs (Figures 6C, D). The gene discussed is STX2; the disease is acute kidney injury.