We hypothesize that: 1) different SAMD9 variants, or variants in different domains of the protein, are associated with milder or diverse endocrine phenotypes, with a focus on adrenal insufficiency; 2) severe gain-of-function of SAMD9 may affect placental function and lead to pregnancy loss and recurrent miscarriage (RM); and that 3) pathogenic variants could be found in children with fetal growth restriction (FGR) as the predominant feature. Here, SAMD9 is linked to spontaneous abortion.