Prior studies have shown that TET2 mutations in hematopoietic stem cells increase the inflammatory properties of myeloid cells, and inflammation plays an important role in ischemic brain damage.[8, 10, 31, 32, 33] Given that TET2 loss of function mutation further complicates the development and function of neutrophils, we examined if neutrophil and eosinophil cell count [(Neu + Eos) #] was a mediator of TET2 on stroke using the INTERVAL consortium (Figure S2A, Supporting Information). The gene discussed is TET2; the disease is Stroke.