Two features make LSD1 inhibition particularly compelling in the venetoclax era: (i) it re-primes mitochondria for apoptosis by increasing BCL-2 reliance, restoring BH3 responsiveness, as demonstrated in preclinical models (Vervloessem et al., 2017); and (ii) its differentiation-led responses, unfolding over weeks, have a lower incidence of fulminant differentiation syndrome (DS: ∼5–10%) compared to IDH or menin inhibitors, supporting outpatient-friendly delivery with cycle-by-count re-dosing and anti-infective prophylaxis (DiNardo and Stein, 2021). This evidence concerns the gene IDH2 and Dravet syndrome.