The genesis of the Landau-Kleffner syndrome gave no clue to the notoriety that would later emerge. In the 1950s, developmental disorders in children were a topic of increasing attention in both medical and educational professions. Kleffner’s institution, Central Institute for the Deaf, had a reputation for its work in teaching speech and language to children who were born deaf. Via Landau, his institution, Washington University School of Medicine, adjacent neighbor of Central Institute, expressed interest in studying the neurologic status of the children enrolled there, most of whom lived in its residential facility. Both institutions quickly found ways to collaborate by setting up a project for obtaining neurologic evaluations and electroencephalography (EEG) studies of all Central Institute children. Among the referrals to Central Institute for the Deaf were several who had developed speech and language normally, only to begin having marked difficulty both in speaking and in comprehending what was said to them. These children were diagnostically puzzling, because although they appeared to be deaf, they had good auditory capacity and had developed normal or near-normal verbal abilities. Kleffner arranged for Landau to pay special attention to these cases. As a result, we were both surprised, Landau because he had never seen such children, and Kleffner because he had no idea that such cases would be unknown to Landau. Recognizing their unique pattern, Landau took the lead in submitting to the journal Neurology the 1957 paper that led to the designation of Landau-Kleffner syndrome (LKS). As part of our introductory presentation at this Symposium, we provided serial films of an early case, Jill, demonstrating her initial symptoms in 1960, her progress a year later after some therapy, and her performance in 2006 as a normally functioning 52-year-old mother of two normal children. Her waking and sleep EEG studies were normal, as was her magnetic resonance imaging (MRI), including state-of-the-art measurement of her temporal lobe cortical thickness. The surprise and honor of the Belgian conclave expanded our hopes for new substantive understanding of our casual observations. Although we deeply appreciate the two dozen contributions documented herein, we must assume the chutzpah of setting forth our wish list of what still needs to be known. Although aphasia is the major disability of this condition, attention has yet to be given to the types, forms, and severity of the speech/language impairments, or to the efficacies of any modes of therapy or retraining for recovery of speech/language functions. To be sure, the use of different forms of communication appropriate for deaf subjects was described, but differences among various approaches for the deaf appeared to be as much influenced by psychosocial philosophies and beliefs regarding the deaf, as by the nature of the language impairment or educational techniques. Evidence regarding the how of education for this disability remains nil. Regarding the epilepsy component of LKS, a major constituent of the syndrome of which we had been unaware is the tremendous exaggeration of paroxysmal brain activity during sleep. We know now that such highly abnormal nocturnal EEGs are also associated with other clinical syndromes, suggestive of predominant paroxysmal activity in other than auditory cerebral territory. But that’s where the descriptive data seem to end. There is no evidence regarding any etiologic relationship between LKS and electroencephalographically similar conditions. We still hope for multiinstitutional efforts to ascertain any significant etiologic factors. Still to be ascertained are cellular histopathology, histochemistry, and channelopathy or other synaptic disturbance. Pathogenesis may possibly be metabolic, genetic, toxic, infectious, or autoimmune. During the era when many new anticonvulsant medications came upon the scene, there have been no systematic efforts even to compare the efficacy of different anticonvulsant medications upon the aphasia symptom. Nor has any ethical or scientific rationale been developed for the non–evidence-based fad of steroid medication. Ill-conceived surgical adventures have failed even to exploit the opportunities for study of LKS brain tissue by any mode. The single report of thin cerebral cortex in the first temporal gyrus of patients with LKS has yet to be confirmed. Our hopeful prayer is that attention to this Symposium and the Epilepsia supplement may mark the graduation of our baby LKS from dictionary curiosity to more productive scientific enterprise. Disclosure: Neither of the authors has any conflict of interest to disclose.