Ovulation and fertilization still occurred in the knock-outs, however remnants of embryos were found in these oviductal diverticula.

[25] In mouse TGFBR-1 knock-in models where a constitutively active TGFBR-1 gene is conditionally induced, the over-activation of the TGFBR-1 receptors lead to infertility, a reduction in the number of uterine glands, and hypermuscled uteri (an increased amount of smooth muscle in the uteri).

[26] Research into how turning off the TGFBR-1 gene affects spinal cord development in mice led to the discovery that, when the gene is turned off, external genitalia instead form as two hind legs.

[27] These experiments show that the TGFB-1 receptor plays a critical role in the function of the female reproductive tract.

They also show that genetic mutations in the TGFBR-1 gene may lead to fertility issues in women.