Two voltage gated sodium channel α-subunits, Na_v1.7 and Na_v1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain. Mis-expression of voltage-gated sodium channels by damaged sensory neurons has also been implicated in the development of neuropathic pain, but the role of Na_v1.7 and Na_v1.8 is uncertain. Here we show that deleting Na_v1.7 has no effect on the development of neuropathic pain. Double knockouts of both Na_v1.7 and Na_v1.8 also develop normal levels of neuropathic pain, despite a lack of inflammatory pain symptoms and altered mechanical and thermal acute pain thresholds. These studies demonstrate that, in contrast to the highly significant role for Na_v1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Na_v1.7 or Na_v1.8 alone or in combination.