However, Sene et al. suggested that presence of B-cell activation markers was lower in non-ataxic sensory neuropathies (ANA, anti-SSA (Ro), anti-SSB (La), RF, hypergammaglobulinaemia) [18], and inversely demonstrated an association between sensorimotor pSS-related neuropathy and higher prevalence of B-cell monoclonal proliferation markers as well as chronic B-cell activation [18, 19], indicating that non-ataxic sensory neuropathies might belong to a subgroup of pSS with a peculiar peripheral sensory neurotropism. The gene discussed is SSB; the disease is peeling skin syndrome.