These studies indicate that the disparity in mortality rates between WDLPS and DDLPS is driven by tumor biology independent of MDM2 or CDK4 amplification, pointing out that our current understanding of WDLPS and DDLPS does not fully address the molecular mechanisms underlying the developmental differences between the two liposarcomas that can be leveraged as therapeutic targets. The gene discussed is CDK4; the disease is dedifferentiated liposarcoma.