Phenotypic plasticity in the form of alterations to teleost skeletons can result from a range of environmental factors, such as the hardness of the prey, particularly when exposure occurs early during development. Determining the molecular underpinnings of teleost skeletal plasticity is hampered by a limited understanding of the molecular basis of bone remodeling in derived teleost fish, whose bones are acellular, lacking the cell type known to orchestrate bone remodeling in mammals. We are using a fitting molecular model for phenotypic plasticity research: the East African cichlid Astatoreochromis alluaudi, with the aim to shed light on the molecular basis of phenotypic plasticity and on the remodeling of acellular bones. For this fish, sustained ingestion of a hard diet induces a 'molariform' lower pharyngeal jaw (LPJ), with molar-like teeth set in an enlarged, relatively dense jaw, while a softer diet results in a smaller, finer 'papilliform' LPJ morphology, representing the 'ground state' for this species. Through comparing genome-wide transcription in molariform and papilliform LPJs, our previous research has shed light on the molecular basis of phenotypic plasticity in the teleost skeleton and by extension, on acellular bone remodeling. In this manuscript we construct a model for the molecular basis of mechanically induced skeletal plasticity in teleosts, which involves iterative cycles of strain and compensatory cellular proliferation. Furthermore, we propose a framework for testing the potential influence of phenotypic plasticity and genetic assimilation on adaptive radiations.