Human peripheral blood lymphocytes stimulated with concanavalin A for 72 h had a 10-fold greater capacity to repair DNA damage induced by N-acetoxy-2-acetylaminofluorene than did unstimulated cells. The increased capacity of concanavalin A-activated cells to repair DNA was not observed after 24 h in culture, a time at which stimulated cells had not begun to synthesize DNA. The maximum rate of repair synthesis obtained after treatment of stimulated cells with the "large patch"-inducing agent, N-acetoxy-2-acetylaminofluorene, was twice that obtained with methyl methanesulfonate, an agent inducing "small patch" repair. The difference between the maximum rates obtained with N-acetoxy-2-acetylaminofluorene and methyl methanesulfonate was 6-fold in a human lymphoblastoid line (cell line RAJI established from Burkitts lymphoma patient). Unstimulated lymphocytes showed almost identical rates of repair after treatment with either N-acetoxy-2-acetylaminofluorene or methyl methanesulfonate. There was close correlation between the rate of N-acetoxy-2-acetylaminofluorene-induced repair synthesis and the loss of acetylaminofluorene adducts from DNA. Treatment of lymphocytes with methyl methanesulfonate led to degradation of cellular DNA with the production of single-stranded regions. Such degradation was not observed with N-acetoxy-2-acetylaminofluorene. The rate of excision repair apparently is a function of the capacity of cells for DNA synthesis and that lymphocytes that do not synthesize DNA have a limited repair capacity and cannot be used to distinguish between large and small patch repair.