Strikingly, 9.2% of childhood AMKL has a genetic background similar to DS–AMKL (DS–AMKL-like: i.e. alterations in genes encoding GATA1, cohesin complex components and signaling effectors together with acquired trisomy 21), with excellent outcome also seen for this subgroup of non-DS children [121]. This evidence concerns the gene GATA1 and Dravet syndrome.