Interestingly, in several cases the emergence of novel chromatin structural features coincides with the genomic location of genes previously associated with cancer, such as TP63 and ANXA3. Whereas the current maps do not allow us to determine cause or consequence for these changes, a broader examination of these changes in larger cohorts of patient samples, together with an integrative analysis of gene expression and chromatin states might provide insight into the causal relationships between these in a disease-specific and patient-specific manner. This evidence concerns the gene TP63 and cancer.