Increasing evidence suggests that ApoE‐ε4 can impede recovery via several mechanisms, including less efficient lipid transport, more beta‐amyloid accumulation, and predisposition to cerebral amyloid angiopathy (Kay et al., 2003; Nicoll, Roberts, & Graham, 1995; Greenberg, Rebeck, Vonsattel, Gomez‐Isla, & Hyman, 1995), increased inflammatory response, and impaired cerebral perfusion (Grocott et al., 2001; Kerr, Kraus, Marion, & Kamboh, 1999), as well as compromised blood–brain barrier and marked cerebral edema (Methia et al., 2001; Lynch et al., 2002). Here, APOE is linked to brain edema.