In the experiments with cell type-specific deletion or overexpression of glucocorticoid receptor (GR) in mice with ischemia, GR signaling in myeloid cells increased Iba-1 (ionized calcium binding adaptor molecule 1) and CD68 (cluster of differentiation 68 protein) staining as well as nuclear p65 (component of nuclear factor kappa-light-chain-enhancer of activated B cells) levels in the injured tissue. This evidence concerns the gene NR3C1 and ischemia.