Vascular endothelial growth factor-A (VEGF-A) is known to promote angiogenesis in solid tumours, and in inflammatory conditions such as arthritis. It is now recognised that VEGF-A is also directly implicated in pain, particularly neuropathic pain such as traumatic, diabetic and chemotherapeutic neuropathy. VEGF-A is alternatively spliced to produce two different families of VEGF proteins – VEGF-Axxxa and VEGF-Axxxb, where xxx denotes the number of amino acids. These differ only in the terminal 6 amino acids, but this difference results in distinct receptor interaction and function. In our studies of the different actions of distinct VEGF-A splice variants, we identified contributions of VEGF-A to nociceptive processes, both peripherally and centrally. Targetting VEGF receptors has potential serious adverse effects on the vasculature, so if a problematic route for development of analgesic drugs based on VEGF-A actions. Taking a step back, and looking at the control of the splicing of VEGF-A, rather than the downstream proteins themselves, we are investigating the possibility of using novel inhibitors of splicing kinases to reverse changes in alternative RNA splicing found in inflammation, cell damage and pain.