In contrast, due to the very low level, virtual lack of NKCC1 expression, the intra-axonal Cl− concentration in nonpeptidergic (IB4-binding) nociceptive primary afferents can be so low that the activation of their GABAA receptors may mediate inward (hyperpolarizing) Cl− currents, which can also lead to the inhibition of the postsynaptic neuronal activity, but cannot generate PAD. The gene discussed is SLC12A2; the disease is peripheral arterial disease.