However, according to Flaherty’s study, both in 66CL4 breast cancer cells and the mouse breast cancer model, GCs can induce DNA damage through an inducible nitric oxide synthase (iNOS)- mediated pathway by increasing levels of nitric oxide (NO); increased NO further stimulated by GC signaling may serve to promote angiogenesis through VEGF in a chronic stress model [30]. This evidence concerns the gene NOS2 and breast cancer.