 Keller (2002) discusses this issue, as well as major features of Turing’s model. One key problem (noted by Waddington at the time) is that “pure homogeneity” as a starting point for development is unrealistic; the egg or early embryo is never a “blank slate” as Turing assumed. She argues that Turing’s was a premature attempt at mathematical biology, noting as well the challenge it posed to prevalent ideas about causality: organismal form as emergent, self-organizing; holistic, arising from the system rather than driven by genes. Vecchi and Hernández (2014) build on Keller’s view, diagnosing “a clash of causal ideologies” in the different possible interpretations of initiating cause in Turing’s model. They are more optimistic about its biological relevance and influence. Scientists continue to apply and reflect on Turing’s model of morphogenesis (e.g., Kondo &amp; Miura 2010). As the latter scholars note, Francis Crick’s source-sink model of embryonic development (1970) can be considered the simplest form of a reaction-diffusion model, with the reaction term removed. However, Crick’s model is mechanistically simpler, with morphogenesis controlled by a single morphogen diffusing along a line of cells: