Peach (Prunus persica cv. Dajiubao) was chosen as a model to clarify the roles of IAA and ABA during the fruit ripening process. Seventy days after flowering (DAF), the fruits were treated with IAA and ABA (0.1 mmol·L?1 and 1 mmol·L?1, respectively) and with the IAA transporter inhibitor (NPA) and the ABA biosynthesis inhibitor (NDGA). IAA decreased the fruit ABA concentration, and increased ethylene concentration, leading to fruit (70 DAF) softening and coloration. NPA had the opposite effect. ABA decreased IAA and ethylene concentrations, leading to fruit hardness and lack of color. NDGA had similar effects as with IAA application. A qPCR analysis indicated that in immature fruits, the expression levels of ethylene biosynthesis and signaling genes (PpACS, PpACO, PpETR, PpERF2), anthocyanin biosynthesis genes (PpCHS, PpDFR, PpF3H, PpUFGT), cell wall softening genes (PpEXP1, PpEXP2, PpPG2, PpPME), and auxin biosynthesis genes (PpPIN, PpTIR1) were upregulated by IAA application but were inhibited by NPA. In contrast, these ripening-related genes were downregulated by ABA application, but upregulated by NDGA. Generally, the immature fruit ripening process requires a high IAA concentration to generate a large amount of ethylene. ABA appeared to modulate ripening through interference not only with ethylene and cell wall related genes but also with auxin-related genes.