Recent studies have shown that fungal growth, development and production of secondary metabolites are regulated by post-translational modifications such as 2-hydroxyisobutyrylation [13]. Expression of A. flavus conidiogenesis genes is regulated by a cascade involving brlA, abaA and wetA [20]. BrlA and abaA are key transcription factors, of which brlA initiates conidia formation, and abaA contributes to conidia development and also affects sclerotia formation and AFB1 production [21,22]. StuA affects the expression of downstream genes by influencing brlA and abaA, and regulates sporulation [23]. VosA, a member of the velvet protein family, co-regulates spore-specific genes with wetA, and is critical for spore maturation and dormancy [24]. Loss of VosA resulted in increased sensitivity to oxidative stress and decreased trehalose content in A. flavus conidia [25]. FluG plays a balancing role in asexual and sexual development, and deletion of fluG can delay and reduce the formation of A. flavus conidia [26]; fluG can also interact with velB or laeA to control the production of conidia and sclerotia [27]. In the present study, the genes wetA, abaA, brlA, stuA, vosA, fluG and con-6 related to conidia were downregulated following deletion of Afngg1, mutant strain colonies were white, conidia production was decreased significantly and the strain no longer produced sclerotia. These results suggest that Afngg1 may regulate developmental balance, oxidative stress and conidia trehalose synthesis, and thereby affect the formation of conidia. Additionally, our experiment found that the ΔAfngg1 strain no longer produced sclerotia, consistent with the results of fluG deletion [27]. Transcriptomic analysis also showed downregulation of genes encoding hydrophobic proteins, namely rodA and dewA, which was confirmed by hydrophobic assay, and is reminiscent of the deletion of laeA in A. flavus [28].