Furthermore, the loss of p53 and thus the ability to repress eIF4E-mediated translation could be a mechanism of the increased cancer risk associated with DBA.261 Indeed, increased eIF4E activity has been shown to promote cellular transformation.262–264 Moreover, RP genes are routinely deleted across human cancers, particularly in concert with TP53 mutations.25 Therefore, inhibitors of cap-dependent translation such as rapamycin and other inhibitors of mTOR may also serve as potential candidates to treat cancers characterized by RP gene deletions and loss of p53. This evidence concerns the gene MTOR and cancer.