Rhizopus stolonifer (R. stolonifer) causing soft rot of sweetpotato resulted in postharvest substantial loss of economy. The antifungal effect and mechanism of cinnamaldehyde (CIN) against R. stolonifer were explored by biochemical analysis and RNA-sequencing in this research, and the edible quality of CIN-treated sweetpotato was evaluated. The results showed that CIN inhibited the growth of R. stolonifer and reduced the incidence of soft rot in sweetpotato at a minimum inhibitory concentration of 1000 μL/L. The damage of cell walls of R. stolonifer by CIN was associated with the up-regulation of CHT1. Cytosolic leakage and malondialdehyde (MDA) content increased following CIN-treatment, which was correlated to higher ROS levels and lower catalase activity. Up-regulation of ERG genes and oxidative stress-related genes following CIN treatment was associated with impaired cell membrane integrity. The mitochondrial structure of R. stolonifer was damaged by CIN treatment resulting in lower respiration rates and ATP production, which was correlated with lower expressions of IDH1, COX4 and QCR7. Our research suggested that the inhibition of CIN on R. stolonifer was related to the disruption of its normal gene expression network. And CIN maintained the nutritional and edible quality of sweetpotato. This study provides valuable insights into the antifungal mechanism of CIN on R. stolonifer and the maintenance of root quality, which contributes to efficient use of CIN on controlling soft rot of sweetpotato.