Correction to: Genet Med advance online publication, 15 June 2018; doi: https://doi.org/10.1038/s41436-018-0013-9.

The author Diva D. De Leon was incorrectly listed as Diva D. De Leó-Crutchlow in the original version of this paper.

Reason for correction of manuscript: Data from Patient 4 and 9 was identified to be derived from the same individual. This patient was born in London, first seen in Great Ormond Street Hospital in London by Dr. Pratik Shah for the initial hyperinsulinism work-up. Subsequently, this patient and her family relocated to the United States and she was seen at Boston Children’s by Dr. Olaf Bodamer where the diagnosis of Kabuki syndrome was made through whole exome sequencing. Unknowingly this patient was aggregated in the data sent from University of Exeter for the manuscript. Due to the initial attribution of the sources from two different geographical locations, the duplication was not detected at the time of manuscript submission. Later the patient was discovered to have been evaluated at both locations and investigations revealed the data duplication.

The following are corrections to our manuscript:

Corrected Title: Congenital hyperinsulinism as the presenting feature of Kabuki syndrome: clinical and molecular characterization of 9 affected individuals

Abstract: In the methods section the total number of patients with HI and KS is nine instead of ten. In the results section, the number of KDM6A pathogenic variants is n=4 instead of n=5.

Main text, page 5, last paragraph of Introduction: Total number of individuals with characterization of presenting features is nine.

Patients and methods: Patient 9 to be removed. Patient 10 will be moved up and renamed as Patient 9.

Results: Clinical details and genetic findings: Patient 9 to be removed. Patient 10 will be moved up and renamed as Patient 9.

Discussion: Nine patients were characterized in the manuscript. Out of the total number of variants identified in KDM6A, two instead of three were truncating variants. Total size of cohort found to have KS and hyperinsulinism (including the case identified from analysis of 100 additional samples) is n=10, with 4 pathogenic variants in KDM6A (40%), which is still an evident enrichment over the general frequency of KDM6A pathogenic variants (2-8%) in KS. Finally, 8 out of 9 of the KS patients with HI were responsive to diazoxide treatment instead of 9 out of 10, reinforcing the same conclusion that the hypoglycemia in these patients were adequately managed with diazoxide, and that a timely diagnosis will be key to improving outcomes.