Type I toxin-antitoxin systems (T1TAs) rely on tight posttranscriptional control to prevent inadvertent toxin synthesis, yet the molecular mechanisms underlying this control are highly diverse. Here, we uncover an RNA-based mechanism that controls translation initiation in the enterobacterial timPR system. Unlike most T1TAs, which typically rely on ribonucleolytic messenger RNA (mRNA) processing to relieve ribosome binding site sequestration, the primary timP toxin mRNA is activated through a pu