As these mutations structurally and functionally mimic the naturally occurring p53-psi isoform, we propose that TP53 exon-6 mutations are best described as 'separation of function' rather than simply 'gain of function' or 'loss of function' Interestingly, approximately one-third of all human genetic disorders are caused by mutations that generate premature stop codons (Frischmeyer and Dietz, 1999). Here, TP53 is linked to hereditary disease.