EETs are rapidly catabolized by soluble epoxide hydrolase (sEH) into less bioactive products such as dihydroxyeicosatrienoic acids (DHETs) (Yu et al., 2000), and the extent of this degradation correlates with deterioration of neurological function, carotid artery stenosis, and plaque instability in patients with cerebral infarction (Yi et al., 2016; Yi et al., 2017). Here, EPHX2 is linked to cerebral infarction.