In agreement with the importance of Kl-mediated activation of the Pi3k-Akt pathway in promoting the meiotic program, a point mutation in the Kit gene, which impairs its interaction with the Pi3k-Akt signaling pathway, causes male sterility owing to a block in the initial stages of spermatogenesis, soon after the beginning of Kit expression.20, 21 Furthermore, male mice expressing a catalytically inactive p110β (the catalytic subunit of Pi3k) develop testicular hypotrophy and impaired spermatogenesis, leading to a phenotype of oligo-azoospermia and defective fertility.22 Here, KIT is linked to Azoospermia.