In phage P4, transcription of the left operon may occur from both the constitutive P_LE promoter and the regulated P_LL promoter, about 400 nucleotides upstream of P_LE. A strong Rho-dependent termination site, t_imm, is located downstream of both promoters. When P4 immunity is expressed, transcription starting at P_LE is efficiently terminated at t_imm, whereas transcription from P_LL is immunity insensitive and reads through t_imm. We report the identification of two nested genes, kil and eta, located in the P4 left operon. The P4 kil gene, which encodes a 65-amino-acid polypeptide, is the first translated gene downstream of the P_LE promoter, and its expression is controlled by P4 immunity. Overexpression of kil causes cell killing. This gene is the terminal part of a longer open reading frame, eta, which begins upstream of P_LE. The eta gene is expressed when transcription starts from the P_LL promoter. Three likely start codons predict a size between 197 and 199 amino acids for the Eta gene product. Both kil and eta overlap the t_imm site. By cloning kil upstream of a tRNA reporter gene, we demonstrated that translation of the kil region prevents premature transcription termination at t_imm. This suggests that P4 immunity might negatively control kil translation, thus enabling transcription termination at t_imm. Transcription starting from P_LL proceeds through t_imm. Mutations that create nonsense codons in eta caused premature termination of transcription starting from P_LL. Suppression of the nonsense mutation restored transcription readthrough at t_imm. Thus, termination of transcription from P_LL is prevented by translation of eta.