BTK and BCL2 inhibitors form the backbone of current CLL therapies.1 Previous studies in aggressive lymphomas and acute myeloid leukemia (AML) have suggested that both drug classes exert some of their cytotoxic effects through ferroptosis induction.16,45 We confirmed this phenomenon in CLL cells and further demonstrated that the first-generation BTK inhibitor ibrutinib enhances ferroptosis sensitivity. This evidence concerns the gene BTK and acute myeloid leukemia.