The tetrodotoxin-resistant sodium channel Na_V1.8/SNS is expressed exclusively in sensory neurons and appears to have an important role in pain pathways^,. Unlike other sodium channels, Na_V1.8 is poorly expressed in cell lines even in the presence of accessory β-subunits. Here we identify annexin II light chain^, (p11) as a regulatory factor that facilitates the expression of Na_V1.8. p11 binds directly to the amino terminus of Na_V1.8 and promotes the translocation of Na_V1.8 to the plasma membrane, producing functional channels. The endogenous Na_V1.8 current in sensory neurons is inhibited by antisense downregulation of p11 expression. Because direct association with p11 is required for functional expression of Na_V1.8, disrupting this interaction may be a useful new approach to downregulating Na_V1.8 and effecting analgesia.