Miscarriage is the most common pregnancy outcome, affecting ~1 in 7 confirmed pregnancies. Despite its prevalence, miscarriage remains shrouded in silence and misconceptions. It is widely believed that chromosome abnormalities are responsible for a large majority of miscarriages. Yet, the transfer of embryos without chromosome abnormalities following in vitro fertilization only offsets the risk of miscarriage partially. In addition, the transfer of embryos with an abnormal chromosome count does not always result in miscarriage, with some embryos being viable until, and even after, birth. Based on my preliminary data, I challenge the long-held view that the genetic causes of miscarriage are limited to chromosomal abnormalities. I hypothesize that the cumulative effect of genome-wide variants in the fetus modulates the risk of miscarriage and modifies the penetrance of chromosome abnormalities. Paradoxically, miscarriage should not be heritable on its own – trade-offs with beneficial traits must exist for this to occur. Thus, fetal variants that increase the risk of miscarriage might be associated with phenotypic traits in cells, embryos and live-born individuals. I will combine family-based study designs, large-scale genomic data sets generated for complex traits, world-unique genetic data from embryos and miscarried fetuses and RNA and imaging data from single cells. This project will pave the way for improving molecular diagnostics of miscarriage and propel the understanding of the fundamental dynamics of early development. We will use personal sensitive data (eg., genotyping array data from miscarried fetuses, preimplantation embryos and their mothers). This proiject has been approved by the Swedish Ethical Review Authority (Dnr-2024-00434-01).