[Background] Mitogen-activated protein kinase (MAPK) signaling pathway of plant pathogenic fungi is involved in sexual reproduction, cell wall integrity, mycelial infection, pathogenicity, stress response and other processes. The MAPK signaling pathway is involved in the growth, development, pathogenicity and stress response in Botrytis cinerea. However, the function of MAPK signaling pathway gene has not been fully elucidated in B. cinerea. [Objective] The objective of this study is to analyze the function of B. cinerea MAPK encoding genes bmp1 and bmp3 in growth, development, pathogenicity and response to oxidative stress, and to lay a foundation for clarifying the molecular mechanism of the MAPK signaling pathway in growth, development and pathogenicity in B. cinerea. [Methods] RNAi mutants of bmp1 and bmp3 genes were successfully constructed using RNAi technology. Compared with the wild-type strain BC22 (WT), phenotype, pathogenicity, and sensitivity to oxidative stress of bmp1 and bmp3 genes RNAi mutants were analyzed. [Results] The colony morphology and mycelia morphology of bmp1 and bmp3 gene RNAi mutants showed no obvious difference with WT. The bmp1 gene RNAi mutants grew slowly and produce fewer conidial. The growth rate of bmp3 gene RNAi mutants showed no obvious difference with WT. The bmp3 gene RNAi mutants did not produce conidia. RNAi mutants of bmp1 and bmp3 genes showed no pathogenicity and penetrating ability. RNAi mutants of bmp1 gene were significantly less inhibited than those of WT in the media containing H2O2, while the degree of inhibition was significantly higher in the media containing menadione than that of WT. RNAi mutants of bmp3 gene were significantly inhibited in H2O2 and menadione media than that of WT. [Conclusion] The bmp1 gene positively regulated growth, conidial formation, pathogenicity and penetrability, and was involved in the regulation of the response to oxidative stress in B. cinerea. The bmp3 gene positively regulates conidial formation, pathogenicity, penetrability, and response to oxidative stress in B. cinerea.