We show herein that a controlled change in the repertoire of VEGF-A alternative splice variants in the environment around peripheral sensory neuronal fibers/terminals, using either exogenous protein or control of endogenous splicing in favor of VEGF-Axxxa, results in enhanced pain, and that VEGF-A165b can alleviate pain in neuropathy. The gene discussed is VEGFA; the disease is neuropathy.