Since ATM was shown to phosphorylate B56γ3 and increase the level of the B56γ3-containing PP2A after DNA damage [45], it is also likely that ATM activation by 5-FU treatment may further increase the B56γ3-containing PP2A to enhance AKT activity to reduce drug sensitivity in CRC cells with stable B56γ3 overexpression. This evidence concerns the gene ATM and colorectal carcinoma.