Historically, mouse models of STEC-HUS analogous to human disease have been challenging to generate possibly due to the lack of glomerular expression of Gb3.5,8 Keepers et al. co-treated C57BL/6 mice with lipopolysaccharide (LPS) and Stx2 to augment Stx-mediated toxicity by proposed cytokine release and found that these mice developed AKI with features of HUS.12 However, this did not happen in isolation in these models, i.e., mice given Stx2 or LPS alone did not develop HUS. This evidence concerns the gene STX2 and hemolytic-uremic syndrome.