ATP6AP2 has been shown to be a multi-functional protein, which is involved in a number of cellular pathways including WNT and MAPK signalling, protein sorting and folding, and receptor-mediated endocytosis and recycling. Many of these functions depend on its interaction with the vacuolar H+-ATPase (V-ATPase). Due to its role in WNT signalling, we hypothesised that ATP6AP2 plays a role in ovarian development. To test this hypothesis, we deleted Atp6ap2 specifically in gonadal somatic cells during fetal development using the Nr5a1-Cre mouse. Surprisingly, these mice appear to develop normally pre-birth, and were born at the expected Mendelian ratio. However, both males and females were infertile. At three months of age conditional Atp6ap2-deficient XY presented with significantly smaller testes caused by the loss of spermatogenic cells. Here we present our data to date regarding the role of ATP6AP2 in testicular somatic cells and how its loss results in male infertility.