The authors suggest that ML-DS progression is influenced by the cooperation between activated signaling pathways and deregulated epigenetic processes in the context of trisomy 21 and GATA1s. For instance, a remarkable co-occurrence of variants in genes encoding tyrosine kinases (e.g., JAK2-3) and RAS proteins with variants in epigenetic regulators (e.g., enhancer of zeste 2, EZH2) or cohesin genes has been shown in ML-DS mouse models and ML-DS patients (Labuhn et al., 2019). Here, EZH2 is linked to Dravet syndrome.