Only a generation ago there were few ideas as to what might cause neuropathic pain, and even fewer relevant data. In contrast, we can currently point to hundreds of distinct cellular changes that are triggered by nerve injury and that might be relevant to the emergence of pain symptomatology. The number may soon increase to thousands. It is essential, therefore, to redirect efforts towards the development of experimental strategies for testing which of these are essential parts of the pain process and which are tangential. In this paper I point out four such strategies: timing, deletion, prevention and genetic heterogeneity, and summarize how one neuropathic pain theory, the ectopic pacemaker hypothesis, holds up to scrutiny.