Interestingly, (C–C-motif) ligand 2 (Ccl2) is induced upon Rbpj deletion since early stages (P5 and P7), is strongly upregulated shortly after Rbpj deletion in vitro (Supplementary Fig. 13h), and is bound by RBPJ (Fig. 7l), suggesting a potential direct role of RBPJ in controlling a pro-inflammatory genetic program in pericytes, which, if activated, is likely to worsen stroke outcome. Here, CCL2 is linked to stroke disorder.