Distinct effects of ATO on G1 and G2 cell cycle checkpoints leading to differences in the extent and duration of the G2/M arrest and the induction of mitotic arrest-associated apoptosis in p53-deficient and p53-proficient cells have previously been reported for the model of multiple myeloma [11] and the Li-Fraumeni syndrome [39] and comparable results were obtained from studies of other DNA-damaging agents such as paclitaxel [40]. The gene discussed is TP53; the disease is AL amyloidosis.