In this context, promising strategies include targeting JAK2 (discussed below); inhibition of MET, whose antichordoma activity has been shown preclinically (35); repurposing DNMT1 inhibitors approved for acute myeloid leukemia; inhibition of PRMT5 in the setting of TBXT-induced MTAP suppression (37, 38); and treatment with cytotoxic drugs that inhibit RRM1 (36), such as gemcitabine. Here, MTAP is linked to acute myeloid leukemia.