JMY is thought to play a dual role in cancer biology by having both a tumor suppressive capacity in the setting of DNA damage where it enhances P53 activity and a tumor metastasis promoter due to its ability to nucleate actin filament.29 Our microarray analysis shows a significant and greater than 2-fold increase in TP531NP expression which suggests that the upregulation of JMY may have been modulating P53 activity in this cell line under the influence of the BFA. Here, TP53 is linked to cancer.