To assess functionality of the TRP53 pathway, we generated cell lines from the primary sgTfap4/Eμ-MYC/Cas9 and sgControl/Eμ-MYC/Cas9 lymphomas and demonstrated by flow cytometry that they are readily killed by treatment with nutlin-3A (a drug that activates TRP53 by blocking its major negative regulator MDM2 [29]) (Fig. 2C), and the DNA-damaging chemotherapeutic drug etoposide (Fig. 2D) that can also kill lymphoma cells through activation of TRP53 [30]. This evidence concerns the gene TP53 and lymphoma.