Given that ROS-generating pro-oxidative stressors can produce oxidized PAF agonists from a variety of PAFR-expressing cell types, which can then travel via the MVP to exert local, as well as systemic effects [34,35,36], the current studies were designed to test our hypothesis if PAFR signaling can modulate targeted therapy-induced MVP release from lung cancer cells, and then define the underlying mechanisms. Here, PTAFR is linked to lung carcinoma.