CXCL12 and stroke disorder: Wang et al. (2014a) showed that after stroke, β3-adrenergic receptor activity reduces the expression of SDF1 in the bone marrow, while the expression of CXCR4 was increased in bone marrow cells. The activated β3-adrenergic receptor also increased the levels of prostaglandin E2 in the bone marrow, which in turn mediates T lymphocyte activation via RANKL (Wang et al., 2014a). Moreover, cationic lipids such as C3a, anaphylatoxin and cathelicidin increase cell responsiveness to low SDF1 gradients, so-called ‘priming’ (Ratajczak et al., 2012).