Underlying disease mechanisms in severe knowlesi malaria include impaired red blood cell (RBC) deformability [9], intravascular haemolysis from parasite-related RBC destruction [10], and endothelial activation mediated by increased osteoprotegerin (OPG) and angiopoietin-2 (Ang-2) levels released from Weibel-Palade bodies [11], all contributing to microvascular dysfunction, impaired perfusion and organ dysfunction [5,12,13]. This evidence concerns the gene ANGPT2 and malaria.