Taking into account the biology of p73 in cancer cells, this pathway can be activated by three broad categories of drugs: 1) compounds that can increase TA-p73 levels, for instance by stimulating its transcription or by inhibiting degradation of the protein, 2) drugs that can modulate the expression or functions of TA-p73 upstream regulators, for instance kinases and acetylases, and 3) molecules that can displace/disentangle p73 from inhibitory interactions with other cellular proteins, most notably ΔN-p73 isoforms and mutant p53. Here, TP53 is linked to cancer.