Our initial hypothesis that podocytes were the target cell for STEC-HUS arose from the seminal work by Eremina et al. in which podocyte-specific knockout of VEGF-A in adult mice resulted in a glomerular TMA.13 Our work suggests that reduced podocyte VEGF-A is also a major driver in STEC-HUS. This evidence concerns the gene VEGFA and hemolytic-uremic syndrome.