The contribution of the MNA clone to the overall tumor behavior in an aggressive genomic environment may be limited and the competition with other subclones may stifle its outgrowth.In line with this assumption, homMNA tumors in our registry rarely occur with 11q deletion and almost never present with a comparable number of aberrations or intragenic ATRX deletions contrary to aggressive hetMNA tumors in >18m patients (Fig. 4). The gene discussed is ATRX; the disease is neoplasm.