In myxoid liposarcoma, the FUS/DDIT3 protein has been shown to upregulate the expression of CCAAT/enhancer binding protein (C/EBP) which leads to the transcription of peroxisome proliferator-activated receptors gamma and other genes involved in adipocytic differentiation. We showed that in myxoid liposarcoma, the atypical NF-kappaB pathway is active. Hereby casein kinase 2 phosphorylates the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (IkB), which releases from the NF-kappaB p50/p65 complex and gets degraded. The NF-kappaB p50/p65 complex then shuttles into the nucleus were it promotes the transcription of genes involved in cell proliferation. Recent studies showed that the FUS/DDIT3 protein facilitates DNA binding of the NF-kappaB p50/p65 complex in a non-direct manner, probably by interfering with IkB. Also Src pathway is activated in myxoid liposarcoma, which leads through different signaling pathways (AKT, MEK, ERK) to tumor growth and cell survival. This pathway can be inhibited in vitro by Src-inhibitor dasatinib.