We speculate that the combined loss of p53 function in response to DNA damage and oncogene (MYC) induced stress may be due to miRNA-mediated regulation of ATM and NLK together with upregulation of TFAP4. Combined, this facilitates survival of eBL tumor cells with the c-myc-Igh chromosomal translocation and promotes MYC induced cell cycle progression initiating eBL lymphomagenesis. The gene discussed is NLK; the disease is neoplasm.