Additionally, somatic mutations in SIX1/SIX2 were found in a subgroup of WT presenting high proliferative potential [19]. Because SIX1 and DROSHA mutations were found to be heterogeneous events within primary tumors, both spatially and temporally, it was speculated if their co-occurrence were positively associated with tumor progression rather than tumor onset [22]. The gene discussed is SIX1; the disease is neoplasm.