The authors concluded that the increased autophagy in the genital tubercles of fetuses exposed to DBP in utero can be due to the inhibition of the PI3K/AKT/mTOR pathway [51] and the activation of the PERK-eIF2α pathway, which can also inhibit apoptosis, promoting the development of DBP-induced hypospadias [52]. This evidence concerns the gene AKT1 and hypospadias.