Genetic and environmental factors are traditionaly seen as the sole causes of congenital anomalies. In this paper we introduce a third possible cause, namely random "manufacturing" discrepancies with respect to "design" values. A clear way to demonstrate the existence of this component is to "shut" the two others and to see whether or not there is remaining variability. Perfect clones raised under well controlled laboratory conditions fulfill the conditions for such a test. Carried out for four different species, the test reveals a variability remainder of the order of 10%-20% in terms of coefficient of variation. As an example, the CV of the volume of E.coli bacteria immediately after binary fission is of the order of 10%. In short, "manufacturing" discrepancies occur randomly, even when no harmful mutation or environmental factors are involved. If the pathway is particularly long or requires exceptional accuracy, output dispersion will be high and may lead to malformations. This effect will be referred to as the dispersion effect. We conjecture that it will be particularly significant when major changes occur; this includes the early phase of embryogenesis or the steps leading from stem cells to differentiated (organ-specific) cells. The dispersion effect not only causes malformations but also innocuous variability. For instance monozygotic (MZ) twins resemble each other but are not strictly identical. It is not uncommon to see only one of the twins of a MZ pair showing a congenital defect (see Appendix A). Not surprisingly, there is a strong connection between congenital defects and infant mortality. In the wake of birth there is a gradual elimination of defective units and this screening accounts for the post-natal fall of infant mortality. For reasons which are not yet fully understood, this fall continues until the age of 10 years. Neither do we understand why, as a function of age, the downward trend of human infant mortality follows a power law with an exponent around 1 (whereas for fish it is about 3, see Bois et al. 2019a). Apart from this trend, post-natal death rates also have humps and peaks associated with various inabilities and defects. In short, infant mortality rates convert the case-by-case and mostly qualitative problem of congenital malformations into a global quantitative effect which, so to say, summarizes and registers what goes wrong in the embryonic phase. Based on the natural assumption that for simple organisms (e.g. rotifers) the manufacturing processes are shorter than for more complex organisms (e.g. mammals), fewer congenital anomalies are expected. Somehow, this feature should be visible on the infant mortality rate. How this conjecture can be tested is outlined in our conclusion.3