Functional studies in FUS-DDIT3 transgenic mice, FUS-DDIT3 murine embryonic fibroblasts, and human liposarcoma cell lines previously demonstrated that FUS-DDIT3 leads to transcriptional downregulation of C/EBPα and PPARγ2 by interfering with C/EBPβ activity, thereby inducing an adipogenic differentiation block [42]. The gene discussed is PPARG; the disease is liposarcoma.