IPS reprogramming and myeloid transdifferentiation of committed B cells have demonstrated the power of the B cell tumor suppressor PAX5 to both maintain B lineage identity and extinguish myeloid programming (Hanna et al., 2008, Xie et al., 2004), yet ETV6-RUNX1 facilitates multilineage priming despite expression of both EBF1 and PAX5 (although at lower levels than control), and so in this regard is exerting a profound effect on lineage regulation. The gene discussed is PAX5; the disease is neoplasm.