Bax, a central cell death regulator, is an indispensable gateway to 
mitochondrial dysfunction and a major proapoptotic member of the B-cell lymphoma 
2 (Bcl-2) family proteins that control apoptosis in normal and cancer cells. 
Dysfunction of apoptosis renders the cancer cell resistant to treatment as well 
as promotes tumorigenesis. Bax activation induces mitochondrial membrane 
permeabilization, thereby leading to the release of apoptotic factor cytochrome 
c and consequently cancer cell death. A number of drugs in clinical use are 
known to indirectly activate Bax. Intriguingly, recent efforts demonstrate that 
Bax can serve as a promising direct target for small-molecule drug discovery. 
Several direct Bax activators have been identified to hold promise for cancer 
therapy with the advantages of specificity and the potential of overcoming 
chemo- and radioresistance. Further investigation of this new class of drug 
candidates will be needed to advance them into the clinic as a novel means to 
treat cancer.