In interpreting their findings, Grivas et al.[9] speculatively applied to TAs the autonomic component of the double neuro-osseous pathogenetic theory for girls with AIS[6], Grivas et al. suggested that severe TAs involve a genetically-determined selectively increased hypothalamic sensitivity to leptin with asymmetry as an adverse hormetic response (hormesis). The gene discussed is LEP; the disease is androgen insensitivity syndrome.