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Conversely, downregulation of CHAC1/BOTCH was associated with increased neuronal damage and impaired recovery ( The regulation of CHAC1/BOTCH involves additional molecular players: during intracerebral hemorrhage, inhibition of CHAC1/BOTCH by the androgen receptor (AR) and Jumonji-domain containing protein-3 (JMJD3) led to elevated NOTCH1 levels and exacerbated neuroinflammation ( ATF4 was most prominently upregulated, though other related genes were also significantly elevated (Yasuda et al., 2014)