With regards to both aforementioned cases of potential experimental confounds, it could be argued that the experimental questions at hand could have been more efficiently and definitively addressed through the genetic manipulation of CD163 and ADAM17 in a murine model of stroke; however, it is becoming increasingly evident that experimental stroke models poorly recapitulate several aspects of pathology51,52, and that in general, immunological responses in laboratory rodents are often poorly analogous to those in humans53,54. Here, CD163 is linked to stroke disorder.