• These preliminary findings highlight substantial genetic heterogeneity in triple-negative

myeloproliferative neoplasms, with recurrent mutations in epigenetic regulators, tumor-suppressor genes

and non-canonical drivers.

• Non-classical JAK2, CALR and MPL variants, together with frequent ASXL1, ARID1B, TET2, TP53 and

RNF145 alterations, warrant further molecular investigation and functional validation in larger matched

cohorts.