Cdkn1a, a gene recurrently altered in T-ALL diagnostic samples through promoter methylation [30] and Nr4a1, a gene involved in clonal deletion of self-reactive T cells during thymic negative selection and in activated T cell exhaustion [31, 32] are up-regulated upon either CnB1 or Nfat inactivation and contribute to ICN1 T-ALL defective LIC properties. This evidence concerns the gene NR4A1 and acute lymphoblastic leukemia.