The Plant Journal (2017) 92, 939–950 **Summary:** This study investigates how plants, specifically petunia flowers, manage the accumulation of phenylalanine (Phe), an aromatic amino acid, which can be harmful in high concentrations. The research focuses on the mechanisms by which petunia flowers reduce Phe levels through the shikimate pathway and vacuolar sequestration. The study shows that by reducing the expression of all three Phe ammonia lyase (PAL) isoforms, which are involved in the non-oxidative deamination of Phe to trans-cinnamic acid, the internal Phe pool in petunia flowers increased by 18-fold. This led to a decrease in the overall flux through the shikimate pathway and a redirection of carbon flux toward the synthesis of aromatic amino acids like tyrosine and tryptophan. The accumulation of Phe did not increase the flux toward phenylacetaldehyde, a compound derived from Phe. Instead, a metabolically inactive pool of Phe was identified, likely localized in the vacuole. The study identified a vacuolar cationic amino acid transporter, PhCAT2, which contributes to the sequestration of excess Phe in the vacuole. In vitro assays confirmed that PhCAT2 can transport Phe, and reducing its expression in PAL-RNAi transgenic plants increased phenylacetaldehyde emission by 1.6-fold. The results demonstrate that plants maintain intercompartmental aromatic amino acid homeostasis through these mechanisms. The study provides critical insights for future strategies in phenylpropanoid metabolic engineering. The findings suggest that plants can sequester excess Phe in vacuoles to prevent its harmful effects, and that this process is regulated by specific transporters. The study also highlights the importance of understanding the metabolic pathways involved in Phe metabolism and the role of vacuolar transporters in maintaining cellular homeostasis.The Plant Journal (2017) 92, 939–950 **Summary:** This study investigates how plants, specifically petunia flowers, manage the accumulation of phenylalanine (Phe), an aromatic amino acid, which can be harmful in high concentrations. The research focuses on the mechanisms by which petunia flowers reduce Phe levels through the shikimate pathway and vacuolar sequestration. The study shows that by reducing the expression of all three Phe ammonia lyase (PAL) isoforms, which are involved in the non-oxidative deamination of Phe to trans-cinnamic acid, the internal Phe pool in petunia flowers increased by 18-fold. This led to a decrease in the overall flux through the shikimate pathway and a redirection of carbon flux toward the synthesis of aromatic amino acids like tyrosine and tryptophan. The accumulation of Phe did not increase the flux toward phenylacetaldehyde, a compound derived from Phe. Instead, a metabolically inactive pool of Phe was identified, likely localized in the vacuole. The study identified a vacuolar cationic amino acid transporter, PhCAT2, which contributes to the sequestration of excess Phe in the vacuole. In vitro assays confirmed that PhCAT2 can transport Phe, and reducing its expression in PAL-RNAi transgenic plants increased phenylacetaldehyde emission by 1.6-fold. The results demonstrate that plants maintain intercompartmental aromatic amino acid homeostasis through these mechanisms. The study provides critical insights for future strategies in phenylpropanoid metabolic engineering. The findings suggest that plants can sequester excess Phe in vacuoles to prevent its harmful effects, and that this process is regulated by specific transporters. The study also highlights the importance of understanding the metabolic pathways involved in Phe metabolism and the role of vacuolar transporters in maintaining cellular homeostasis.