Aspergillus flavus accumulates carcinogenic aflatoxins in peanuts, mainly in immature kernels during drought. Aspergillus flavus invasion induces accumulation of phytoalexins, mostly stilbenoids in peanut, as a plant defence mechanism. Because fungal laccases are often related to pathogenicity and can degrade stilbenoids, this study reports for the first time the expression of A. flavus laccases in the presence of kernels, hulls and low water potential in relation to the accumulation of phytoalexins in peanut kernels. Packed-cell volume (PCV) of A. flavus biomass was significantly higher (P ≤ 0·01) in the presence of mature kernels, dead kernels, and mature and immature peanut hulls than the control. The presence of kernels and hulls lowered the level of expression of three A. flavus laccases by 4–6-fold (P < 0·01), whereas 3% sucrose up-regulated them by 35–304-fold, and low water potential (−1·1 MPa) up-regulated them by 85–248-fold (P < 0·01). Phytoalexins that accumulated in peanut kernels in the presence of A. flavus and were quantified by HPLC-DAD-MS were primarily the stilbenoids: 3′-isopentadienyl-3,5,4′-trihydroxystilbene (IPD), chiricanine-A, arachidin-2, arachidin-3 and arahypin-1. Apparent degradation of phytoalexins was observed when using a priori induction of phytoalexins in seeds in combination with a priori induction of laccases in A. flavus. The up-regulation of laccase expression observed at −1·1 MPa and at high sucrose concentration could be contributing to peanut invasion in immature kernels under drought conditions.