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Our data demonstrate that the VAD\u2010induced testicular degeneration arises through the normal maturation of germ cells in a context of spermatogonia differentiation arrest. They indicate that retinoic acid (RA) appears dispensable for the transition of premeiotic to meiotic spermatocytes, meiosis, and spermiogenesis. They confirm that RA plays critical roles in controlling spermatogonia differentiation, spermatid adhesion to Sertoli cells, and spermiation, and suggest that the VAD\u2010induced arrest of spermatogonia differentiation results from simultaneous blocks in RA\u2010dependent events mediated by RA receptor \u03b3 (RAR\u03b3) in spermatogonia and by RAR\u03b1 in Sertoli cells. They also provide evidence that expression of major RA\u2010metabolizing enzymes is increased in mouse Sertoli cells upon VAD and that vitamin A\u2010deficient A spermatogonia differ from their RA\u2010sufficient counterparts by the expression of the <jats:italic>Stra8<\/jats:italic> gene. 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