The oxLDL interaction with CD36 on the surface of a platelet triggers a signaling cascade involving specific SFK, syk, MAPK c-Jun N-terminal kinase, Vav-family guanine nucleotide exchange factors, and PLCγ2, leading ultimately to the activation of the NOX2 isoform of NADPH oxidase and generation in intracellular ROS, including superoxide ion. This pathway leads directly to platelet activation and secretion, and the studies by Magwenzi et al showed that ROS also contribute to platelet activation by inhibiting the NO/cGMP/PKG pathway that normally serves as an inhibitor or “brake” on platelet activation.