ENO1 and systemic lupus erythematosus: This may imply that HE pathogenesis is either due to vasculitis, as alpha-enolase has been described in other autoimmune vasculitides such as SLE, ANCA, and RA, or due to global cerebral hypoperfusion, as a consequence of disruption of the brain endothelium, where alpha-enolase is highly expressed [15].