The predictors of DS were represented by a higher leukemic burden in the bone marrow (≥48% of blasts) and in the blood (≥15–25% blasts); furthermore, concurrent mutations in TET2 and SRFSF2 were associated with a higher risk of developing DS, and the CR + CRi rates were lower in the patients with versus those without DS (Ivosidenib 18% vs. 36%; Enasidenib 18% vs. 25%) [65]. Here, TET2 is linked to Dravet syndrome.