While the recent studies by Maria-Riera et al suggest that the TP53R248Q mutation primarily confers self-renewal and survival capabilities by repressing known p53 targets, rather than directly impacting erythroid differentiation,[12] complete abrogation of p53 function, often associated with frameshift, nonsense, or splice site mutations, appears to be crucial for full-blown PEL development.[12] In our specific case, the identified TP53 frameshift mutation leading to null p53 expression potentially represents the underlying molecular mechanism and driving force of PEL development. Here, TP53 is linked to primary effusion lymphoma.