In the intracerebral hemorrhage model, the Cx43 mimetic peptide Gap19 suppresses both the abnormal protein expression of Cx43 and the excessive opening of Cx43 hemichannels without Cx43 transcription in astrocytes, facilitates YAP-dependent SOCS1 and SOCS3 expression, and then inhibits two inflammatory signaling pathways, the toll-like receptor 4/NFκB and Janus kinase 2/STAT3 pathways, to protect cell survival against reactive astrocytes after intracerebral hemorrhage [121]. This evidence concerns the gene GJA1 and intracerebral hemorrhage.