Synaptojanin and ITSN1 overactivity, associated with neuronal loss, atrophic basilar dendrites, and atypical synaptic density, disrupt neuronal migration and synaptic transmission in the developing brain with DS by defective endocytic processes, elevating Ras activation and increasing neuronal receptor trafficking and neurodegeneration (Pucharcós, 1999; Arai et al., 2002), which may disrupt normal brain functioning and cause the development of ID in DS. Here, ITSN1 is linked to Dravet syndrome.