The mechanistic dichotomy of NETosis enables pathway-specific nanomedicine strategies, with ROS-dependent suicidal NETosis inhibited by NADPH oxidase inhibitors (e.g., diphenylene iodonium, DPI) or ROS scavengers targeting NOX2 activity, whereas Ca2+-dependent vital NETosis is selectively suppressed via TLR2/4 antagonists or PAD4 inhibitors (e.g., GSK484), thereby offering dual therapeutic avenues to modulate pathological NETs formation in inflammatory or tumor microenvironments [50]. This evidence concerns the gene PADI4 and neoplasm.