 Are there problems with claiming that genes contain all of the information (see the entry on  biological information)  to form vertebrate hearts? Is there a genetic program in the DNA controlling heart development? Are genes the primary supplier and organizer of material resources for heart development, largely determining the phenotypic outcome? Existing studies of heart development have identified a role for fluid forces in specifying the internal form of the heart (Hove et al. 2003) and its left/right asymmetry (Nonaka et al. 2002). Biochemical gradients of extracellular calcium are responsible for activating the asymmetric expression of the regulatory gene Nodal (Raya et al. 2004) and inhibition of voltage gradients scrambles normal asymmetry establishment (Levin et al. 2002). Mechanical cues such as microenvironmental stiffness are crucial for key transitions from migratory cells into organized sheets during heart formation (Jackson et al. 2017). A number of genes are clearly difference makers in these processes (Asp et al. 2019; Srivastava 2006; Brand 2003; Olson 2006), but the conclusion that genes carry all the information needed to generate form features of the heart seems unwarranted. While it may be warranted empirically in some cases to privilege DNA sequence differences as causal factors in specific processes of ontogeny (Waters 2007a), such as hierarchically organized networks of genetic difference makers explaining tissue specification (Peter and Davidson 2011), the diversity of entities appealed to in molecular genetics and the extent of their individual and joint roles in specifying developmental outcomes implies that debates about the meaning, scope, and power of genetic explanations will continue (Griffiths and Stotz 2013). However, a shift away from genetic programs and genetic determinism to DNA, RNA, and proteins as difference makers that operate conjointly suggests that we conceptualize other causal factors in a similar way.