Support for this assumption comes from studies showing that the homologous protease PfHtrA2 similarly fulfils a non-protease/chaperone role in the life cycle of the human malaria parasite Plasmodium falciparum [69], that HtrA2/Omi itself prevents the aggregation of amyloid β1-42 in a protease-independent manner by acting as a chaperone protein [16], or that the protease-activity of HtrA2/Omi is not required to induce apoptosis in Apollon/BRUCE-deficient cells [24]. The gene discussed is HTRA2; the disease is malaria.