Although the identity and mechanisms of regulators of TAp73-mediated c-Jun phosphorylation have yet to be unraveled, it is emerging that TAp73, which is overexpressed in cancers, causes c-Jun phosphorylation and thus could result in the recruitment of specific AP-1 members that would altogether cooperate in the activation of AP-1 target genes (Fig. 8E). The gene discussed is FOS; the disease is cancer.