Given that STI-1 is a proposed ligand for PrPC (Martins et al, 1997; Zanata et al, 2002) and that PrPC is also upregulated following stroke (Weise et al, 2004), the increase in STI-1 would undoubtedly complement the increase in PrPC, resulting in a substantial increase in STI-1-to-PrPC signalling following stroke. This evidence concerns the gene STIP1 and Stroke.