Different wild-type strains of Drosophila melanogaster display variation in the ability to resist the toxic effects of continuous development from the egg stage on media supplemented with aflatoxin B1 (AFB1, a potent insect toxigenic agent and vertebrate hepatocarcinogen). The genetic basis of differences in egg-pupa development time and egg-adult viability have been investigated by chromosome substitution analysis. Five strains were studied: A-11, a "resistant" strain showing relatively little effect from the AFB1 treatments, with increased development time, reduced viability, and smaller body size); and three strains produced by chromosomal substitution from A-11 and A-9, testing the effect of either chromosome X (strain R-X), 2 (strain R-2) or 3 (strain R-3) from A-11 against an A-9 background. Data from R-X, R-2, and R-3 indicate that autosomal genes on chromosomes 2 and 3 control the ability of strain A-11 to resist the toxic effects of AFB1 ingestion during larval development.