On the other hand, disrupted interactions involving TFs and target genes that maintain expression levels in normal and tumor cells may be attributed to multiple reasons: presence or absence of a third-party molecule that could be acting as a post-translational modulator of the TF activity (i.e. phosphorylation, acetylation, ubiquitination) [36], alteration of key co-factors [1], or alterations in promoter regions that could create new TF-binding sites in target genes [37, 38]. Here, TF is linked to neoplasm.