Even so, the absence of the SRY gene or the silencing of the SOX9 gene are not enough to trigger sexual differentiation of a fetus in the female direction. One X chromosome gives putative maleness. In these cases, the SOX9 gene, involved in the development of testes, can induce their development without the aid of SRY. However, In an interview for the Rediscovering Biology website,  researcher Eric Vilain described how the paradigm changed since the discovery of the SRY gene: Many insects of the order Hymenoptera instead have a system the haplo-diploid sex-determination system , where the males are haploid individuals which have just one chromosome of each type , while the females are diploid with chromosomes appearing in pairs. Some other insects have the X0 sex-determination system , where just one chromosome type appears in pairs for the female but alone in the males, while all other chromosomes appear in pairs in both sexes. It turns out that the sex determination pathway is probably more complicated and SRY may in fact inhibit some anti-male genes. After the discovery of the testis-determining gene SRY , many scientists shifted to the theory that the genetic mechanism that causes a fetus to develop into a male form was initiated by the SRY gene, which was thought to be responsible for the production of testosterone and its overall effects on body and brain development. Aristotle claimed that the male principle was the driver behind sex determination,  such that if the male principle was insufficiently expressed during reproduction, the fetus would develop as a female. In this process, an X chromosome and a Y chromosome act to determine the sex of offspring, often due to genes located on the Y chromosome that code for maleness.