Ten percent of inherited diseases are caused by premature termination codon 
(PTC) mutations that lead to degradation of the mRNA template and to the 
production of a non-functional, truncated polypeptide. In addition, many 
acquired mutations in cancer introduce similar PTCs. In 1999, proof-of-concept 
for treating these disorders was obtained in a mouse model of muscular 
dystrophy, when administration of aminoglycosides restored protein translation 
by inducing the ribosome to bypass a PTC. Since, many studies have validated 
this approach, but despite the promise of PTC readthrough therapies, the 
mechanisms of translation termination remain to be precisely elucidated before 
even more progress can be made. Here, we review the molecular basis for PTC 
readthrough in eukaryotes and describe currently available compounds with 
significant therapeutic potential for treating genetic disorders and cancer.