In particular, parental mutations in genes involved in the RNA editing pathway, such as the cytidine deaminase Apobec1 (ApoB editing complex 1) (Nelson et al. 2012) and the RNA-binding proteins Dnd1 (Deadend1) (Lam et al. 2007; Nelson et al. 2012), A1cf (APOBEC1 complementation factor) and Ago2 (Argonaute2) (Carouge et al. 2016) modify offspring’ risk of testicular diseases, including atrophy, cryptorchidism, and testicular germ cells tumor in a genotype and parent-of-origin specific manner. This evidence concerns the gene AGO2 and testicular disorder.