 At other times, statements concentrate on genetics as the primary locus of causation in ontogeny: “Developmental complexity is the direct output of the spatially specific expression of particular gene sets and it is at this level that we can address causality in development” (Davidson and Peter 2015: 2). Whether or not these statements can be substantiated has been the subject of intense  debate.[12]  The strongest claims about genetic programs or the genetic control of development have empirical and conceptual drawbacks that include an inattention to plasticity and the role of the environment, an ambiguity about the locus of causal agency, and a reliance on metaphors drawn from computer science (Gilbert and Epel 2009; Keller 2002; Moss 2002; Robert 2004). However, this leaves intact the difference-making principle of genetic explanation exhibited in molecular genetics (Waters 2007a), which yields more narrow and precise causal claims under controlled experimental conditions, and is applicable to diverse molecular entities that play causal roles during development, such as regulatory RNAs, proteins, and environmental signals. We can observe this briefly by reconsidering the example of vertebrate cardiogenesis  (Section 1.2).