Mutation in the CREBBP could cause C-terminal truncation in the HAT domain or change the amino acid residue(s), which weakens its capacity of acetylating BCL6 and p53 which are its substrates, in turn resulting in the activation of oncoprotein and reduced tumor suppressive role of p53 for the regulation of the DNA damage response reaction which occurs in the germinal center during immunoglobulin genes remodeling [59]. Here, TP53 is linked to neoplasm.