Likewise, Nicholas Shea’s Millikan-derived analysis does not seem to map naturally onto independently specifiable biological mechanisms. For him, the sender of genetic messages is natural selection operating on and filtering the gene pool of a population; messages are read by the developmental system of the organism as a whole (Shea 2013). But the less clearly a sender-receiver or producer-consumer framework maps onto independently recognised biological mechanisms, the more plausible a fictionalist or analogical analysis of that case becomes. So we see an important difference between a reader being the developmental system as a whole, and reader being a receptor on a cell membrane. The cell-level machinery of transcription and translation (the ribosomal/tRNA machinery, especially) really is a reader or consumer of nucleic acid sequences, with the function of creating protein products that will have a variety of uses elsewhere in the cell. But this realization of the causal schematism applies only at the cell level, at the level at which the transcription and translation apparatus shows up as a definite part of the machinery. One of the most extraordinary features of ontogeny is that it proceeds reliably and predictably without any central control of the development of the organism as a whole. There is nothing, for example, that checks whether the left-side limbs are the same size as the right side limbs, intervening to ensure symmetry. Similarly, there are DNA sequence-readers, and some intercellular sender-receiver systems with clear “readers” (such as neural structures), but there are no higher-level readers that interpret a message specifying the structure of a whole limb-bud in the embryo.