In addition, five mutations (out of 73 T-ALL patients) were identified in the cyclin-C/CDK recognition sites in the Cdc4 phosphodegron of Notch1 leading to ICN1 stabilization and were able to enhance T-ALL development when reproduced in mouse models, supporting the notion that alteration of the cyclin-C/CDK-dependent regulation of Notch1 contributes to human leukemia (Li et al., 2014). The gene discussed is CCNC; the disease is acute lymphoblastic leukemia.