Another potential experimental confound lies in our use of Marimastat to inhibit ADAM17 in vitro; because Marimastat has activity against multiple proteases (MMP1, MMP2, MMP3, MMP7, MMP9, and MMP14 in addition to ADAM17)50, it is possible that the ablation of stroke serum-induced monocytic sCD163 production we observed upon treatment with Marimastat was the result of the inhibition of a shedase other than ADAM17. The gene discussed is ADAM17; the disease is stroke disorder.