Therefore, cyclin C/CDK3/CDK8/CDK19 complexes function as tumor suppressors in T-ALL by preventing the accumulation of ICN1 and the lack of these complexes led to enhanced T-ALL development in Lck-LMO1 transgenic mice that mimic the alterations found in human T-ALL (Li et al., 2014). The gene discussed is CCNC; the disease is acute lymphoblastic leukemia.