As peptide Aβ (1-42), by aggregating in cross-β-structured fibrils, with a similar conformation as fibrin peptides, could substitute for fibrin in the activation of tissue plasminogen activator (tPA) (Kingston et al., 1995), and because plasmin cleaved peptide Aβ 1-40 into a truncated form, with potent stimulatory activity toward tPA (VanNostrand and Porter, 1999), it was proposed that the loss of plasminogen-binding activity of HNE-α-enolase might foster apoptosis in AD, by hindering Aβ peptide degradation (Sultana et al., 2012). The gene discussed is PLG; the disease is Alzheimer disease.