Therefore, it is likely that the upregulation of AP4 expression also mediates cell cycle progression, probably in response to MYC activation, coupled with P53 loss of function due to miRNA regulation of ATM and NLK, would facilitate the survival of cells harboring the c-myc-Igh translocation initiating eBL tumor development (Fig. 5). The gene discussed is TP53; the disease is neoplasm.