In alcohol-induced neuropathy, protein kinase Cε(PKCε) has a major contribution to mechanical hyperalgesia [2], whereas in AIDS therapy neuropathy, Ca++, caspase signaling and mitochondrial electron transport [3-5] but not PKCε or a number of other second messenger signaling pathways (i.e., protein kinase A, protein kinase G, extracellular signal-regulated kinases 1/2 or nitric oxide) contribute [3]. The gene discussed is PRKCE; the disease is neuropathy.