Researchers disclosed that altered sphingolipid metabolism driven by ASAH1 contributes to venetoclax resistance in acute myeloid leukemia, particularly in monocytic phenotypes. The BMC Cancer study mapped metabolic shifts that reduce venetoclax sensitivity and identified ASAH1 as a potential target to reverse resistance. The finding provides a mechanistic route to combine metabolic inhibitors with BCL‑2 blockade. Drug developers and clinical teams may use these data to prioritize ASAH1 modulators or biomarker-driven trials aimed at overcoming venetoclax failure in AML subtypes.