CAMK4 and Ataxia: In the present study, we adopted an unbiased trio WES strategy to discover a de novo heterozygous CAMK4 consensus splice-site alteration (c.981+1G>A) as the only suspicious finding in a proband who manifested a remarkable spectrum of neurodevelopmental deficits including global psychomotor delay, intellectual disability, autistic traits, adolescence-onset hyperkinetic movement disorder, ataxia, and cerebellar atrophy.