The dominant theory of sexual differentiation of the brain holds that sex differences in brain anatomy and function arise because of the action of gonadal steroids during embryonic and neonatal life. In mammals, testicular steroids trigger masculine patterns of neural development, and feminine patterns of neural development occur in the absence of such testicular secretions. In contrast, gonadal differentiation in mammals is not initiated by hormonal mechanisms, but is regulated by the action of gene products such as SRY, a testis-determining gene on the Y chromosome. This paper argues that such genetic, nonhormonal signals may also trigger specific examples of sexual differentiation of the brain. This thesis is supported by two arguments. The first is that "direct genetic" (i.e., nonhormonal) control of sexual differentiation may be as likely to evolve as hormonal control. The second line of argument is that neural and nonneural dimorphisms have already been described that are not well explained by classical theories of steroid-dependent sexual differentiation and for which other factors need to be invoked.