The p53 tumor suppressor is part of a small family of related proteins that 
includes two other members, p73 and p63. Interest in the p53 family members, 
their functions and their complex interactions and regulation, has steadily 
grown over recent years and does not show signs of waning. p73 is a major 
determinant of chemosensitivity in humans, and mutant p53 proteins carrying 
specific polymorphisms can induce drug resistance by inhibiting TAp73. 
Cooperation between TA (transactivating, proapoptotic, antiproliferative) and 
Delta N (truncated, antiapoptotic, pro-proliferative) p73 isoforms and among the 
three family members guarantees equilibrium between proliferation, 
differentiation, and cell death, thus creating a harmony that is lost in several 
human cancers. In this article, we review our current knowledge of the role of 
p73 in cancer chemosensitivity and the real prospect of therapy targeting this 
molecule. We also draw attention to the crucial role of specific phosphorylation 
and acetylation events for p73-induced apoptosis and drug chemosensitivity.