Chromosomal translocation is one of the most important events in leukemogenesis of childhood B-precursor acute lymphoblast leukemia (ALL), and its significance in disease prognosis has been well documented. p53 is critical regulator of cell death, cell cycle progression, and DNA repair, and, recently, its critical involvement in the efficiency of induced pluripotent stem cell generation was documented [1] . Of note, TP53 mutation is widely observed in various tumors including leukemia. An early retrospective study of exons 5-8 of the TP53 gene in 50 B-precursor ALL cases demonstrated that only one case (2%) had mutation [2] , and a large retrospective study of 264 childhood B-precursor ALL cases at diagnosis demonstrated that only five cases (1.9%) had TP53 mutation in exons 5-8, which encode highly conserved regions during evolution [3] . The incidence of TP53 mutation in exons 4-9 among poor-outcome childhood ALL cases at diagnosis was 30% (3/10 cases) [4] . Later studies reported that TP53 mutation might be relatively frequent among ALL with MLL-rearrangement and t(1;19): the inci-dence of TP53 mutation in exons 5-9 in MLL-rearranged ALL at diagnosis was 23% (3/13 cases) [5] , and that in exons 2-11 in t(1;19)-ALL at diagnosis was 10% (2/20 cases) [6] . In contrast, TP53 mutation was rare in Philadelphia chromosome (Ph1)-positive ALL: none of 15 Ph1-positive ALL cases at diagnosis had TP53 mutation in exons 2-11 [7] . Although these reports suggest correlation of TP53 mutation with the type of chromosomal translocation in childhood B-precursor ALL, it has not been directly confirmed in a single cohort study due to the limited incidence of TP53 mutation in primary samples at diagnosis. Leukemia cell lines are usually established from leukemia in progressed disease status, and, thus, generally show higher incidence of gene mutations compared with primary samples [8] . In fact, Kawamura et al. [6] reported that the incidence of TP53 mutation was increased to 80% (4/5 cell lines) among t(1;19)-ALL cell lines, suggesting that the incidence of TP53 mutation might be augmented in cell lines. Accordingly, ALL cell lines would be useful tools to confirm the correlation of TP53 mutation with chromosomal translocations.