Protein p53 has a central role in tumor suppression. Under normal conditions, p53 levels are kept low, but in response to DNA damage, p53 becomes stabilized and initiates the transcription of its target genes. In chronic lymphocytic leukemia (CLL), aberrations in the TP53 gene are associated with the aggressive disease since the function of p53 protein is impaired. However, the p53 function might also be disrupted by other mechanisms, e.g. altered phosphorylation, even in the wild-type protein. Therefore, we aimed to investigate the impact of p53 phosphorylation on p53 function in CLL and uncover what underlies the existence of possible different phosphorylation patterns.