If future clinical studies can demonstrate an adverse prognostic impact of high endocan levels at the time of diagnosis in AML and/or ALL, this would support further clinical studies of endocan-inhibitory therapeutic strategies (e.g., inhibition of endocan expression or downstream intracellular signaling (Table 1), antibody blocking of the N-terminal part [20]). The gene discussed is ESM1; the disease is acute myeloid leukemia.