Only a generation ago there were few ideas as to what might cause neuropath
ic pain, and even fewer relevant data. Ln 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 nu
mber may soon increase to thousands. It is essential, therefore, to redirec
t efforts towards the development of experimental strategies for testing wh
ich of these are essential parts of the pain process and which are tangenti
al. In this paper I point out four such strategies: tin-Ling, deletion, pre
vention and genetic heterogeneity, and summarize how one neuropathic pain t
heory, the ectopic pacemaker hypothesis, holds up to scrutiny.