Indeed, human neurons with a defective CDKL5 gene had reduced numbers of synapses and long dendritic protrusions, as seen in mouse hippocampal neurons with knock-down of Cdkl5. Although the proposed mechanism was not fully addressed in human neurons, evidence from iPSC-modeling supports that the functional defect due to loss of CDKL5 in affected individual results in disease-related phenotypes similar to RTT. This evidence concerns the gene CDKL5 and Rett syndrome.