[Objective] Anthracnose is a major disease attackingCamellia oleifera plants.Colletotrichum fructicola with a wide distribution scope and a high isolation rate is the major pathogen causing anthracnose inC.oleifera. This study explored the roles of autophagy-related proteins CfAtg6 and CfAtg14 and the molecular mechanism for the pathogenicity ofC.fructicola, aiming to provide a theoretical basis for the prevention and control of anthracnose inC.oleifera. [Methods] The homologous recombination principle and polyethylene glycol (PEG)-mediated transformation method were employed to construct the gene-deleted strains ΔCfATG6 and ΔCfATG14 and the complemented strains ΔCfatg6-C and ΔCfatg14-C. [Results] The yeast two-hybrid assay results showed that ΔCfatg6 and ΔCfatg14 might interact with each other. Compared with the wild type and complemented strains, ΔCfatg6 and ΔCfatg14 demonstrated significantly slow vegetative growth, and their appressorium formation rates were only 5% and 18% that of the wide type. In addition, ΔCfatg6 and ΔCfatg14 showed significantly weakened pathogenicity, causing the lesion areas only 1/3 of the wild type and complemented strains onC.oleifera leaves. In addition, ΔCfatg6 and ΔCfatg14 lost the ability of transporting and degrading CfAtg8 protein and became more sensitive to the cell wall stress. The conidium production of ΔCfatg6 decreased significantly, being only 20% that of wild type. The inhibition rate of hydrogen peroxide on the growth of the deleted strains was 10% higher than those on the wild type and complemented strains. ΔCfatg14 showed increased sensitivity to dithiothreitol stress. [Conclusion] The autophagy-related genesCfATG6 andCfATG14 are involved in the regulation of the growth, autophagy, and pathogenicity ofC.fructicola.