At mechanistic level, their findings that the reintroduction of PAX5 into REH cells induced cell cycle arrest and resulted in a more drug-resistant phenotype [36] were consistent with previous mouse study by Somasundaram et al. [35] that explored the MYC/PAX5 axis in pro-B cell development and B-cell acute lymphoblastic leukemia. The gene discussed is PAX5; the disease is B-cell acute lymphoblastic leukemia.