The results obtained in case 1 clearly suggest a role as a tumor suppressor (TS) gene not only for RUNX1 (the shorter RUNX1 encoded by the chimeric RUNX1/UBL7-AS1 should behave as a dominant negative mutant of the wild-type RUNX1), but also for SIN3A. We speculate that the inactivation of both proteins should have led to an abnormal activation of RUNX1/SIN3A target genes, leading to myelodysplasia. The gene discussed is RUNX1; the disease is Myelodysplasia.