Both reports described that most common alterations were in cell cycle control, p53 and Rb1, receptor tyrosine kinase/PI3K in addition to the low frequencies of both tumor mutational burden and microsatellite instability, and several subtype-specific associations such as SAMRCB1 deletion in epithelioid sarcoma and malignant rhabdoid tumor as well as cyclin-dependent kinase 4 (CDK4) and mouse double minute 2 homolog (MDM2) amplification in well/dedifferentiated liposarcoma. This evidence concerns the gene CDK4 and liposarcoma.