Glycolipids (GL) have been implicated as potential antigens in autoimmune neuropathies, but their role in paraneoplastic neuropathy has been poorly investigated. We describe two patients affected by lung neoplasia and subacute sensori‐motor axonal neuropathy with high titres of IgG auto‐antibodies against GM1, GD1b, GQ1b, GD1a, GD2, GM2, GM3, GD3, asialo‐GM1 and sulfatide. The first patient showed prevalent sensory axonal neuropathy, ophthalmoplegia and dysphagia. Small cell lung carcinoma was bioptically discovered and treated with chemotherapy and irradiation, which yielded clinical stabilization and decline of anti‐GL IgG titre in a two years follow‐up. The second patient complained of subacute, progressive distal hypostenia. Neurologic examination showed areflexic, hypotonic tetraparesis with marked wasting, fasciculations, mimicking lower motor neuron disease. In addition to anti‐GL IgG, we detected expansion of peripheral γ/δ T lymphocytes (3% of total T cells, n.v. <0.5%), a T cell subset known to recognize lipid antigens. Lung adenocarcinoma was discovered and surgically removed. After two months, neuropathy stabilized and both anti‐GL IgG and γ/δ T lymphocytes markedly declined. Immunohistochemistry on this patients' tumor showed expression of GM1, GD1a, GD2, GM2, GM3, GD3 on neoplastic cells, which were infiltrated by IgG and CD8 and γ/δ T lymphocytes. The association of neoplasia, peripheral neuropathy and autoimmune responses to GL observed in our patients proposes a previously underestimated role for GL as putative antigens in paraneoplastic neuropathy. GL should be considered as candidate antigens in paraneoplastic neuropathy and anti‐GL IgG should be evaluated in patients with subacute sensory and/or motor neuropathy.