A radioimmunoassay (RIA) to detect antibodies against what was initially believed to be voltage-gated potassium channels (VGKC) in patients with neuromyotonia was established 20 years ago.¹ The rationale for this test came from previous RIA assays that detected antibodies against acetylcholine receptors or voltage-gated calcium channels in which the antigens were labeled with ¹²⁵I-specific neurotoxins and precipitated with patients' antibodies.¹ It was soon clear that the results of the VGKC RIA were very different from those expected based on the achievements of the RIA for the antibodies associated with myasthenia gravis and the Lambert-Eaton syndrome. First, only a minority of patients with neuromyotonia, the initial disease target of the VGKC RIA, were positive. Second, high levels of VGKC antibodies were found in a subset of patients with nonparaneoplastic limbic encephalitis and good response to immunotherapy.² Third, it was known by 2004 that low levels of VGKC antibodies occurred in 5% of subjects without neurologic disorders.² However, no recommendations on the clinical value, if any, of these low-positive VGKC antibody levels were provided until a decade later.^3,4 Finally, as the VGKC RIA test became more widely available, the type of clinical syndromes reportedly associated with these antibodies increased exponentially in both adults and children.^3–5