In recent years, many molecular endocrine mechanisms that regulate tissue morphogenesis have been detailed in laboratory amphibian models. However, most of these pathways have not been examined across more closely related species to understand how deviations in endocrine pathways may have contributed to amphibian diversification. The timing of metamorphosis and maturation vary extensively across plethodontid salamanders (including direct developing, biphasic, and paedomorphic species), making them an ideal system for analyzing the evolution of endocrine mechanisms in a phylogenetic context. Recent phylogenetic-based reconstructions concluded that ancestral plethodontids were likely direct developers, and free-living larval periods were independently derived multiple times within this family. Furthermore, within one clade (Spelerpini) there have been multiple independent transitions from biphasic (metamorphic) to paedomorphic developmental modes. This inspires the question: What endocrine/developmental mechanisms govern these extreme life history transitions? Prior endocrine models for the evolution of direct development and paedomorphosis have been largely based on the ontogenetic timing of thyroid hormone release and/or thyroid hormone responsiveness of target tissues. Here I review endocrine pathways that influence metamorphosis and maturation in laboratory amphibians (Clawed frog and Axolotl) and other species, and develop a model that integrates prior thyroid hormone-based patterns with other endocrine axes. This integrated framework incorporates developmental shifts that result from plasticity or evolution in the timing of hatching, metamorphosis, and maturation, and can be used to test mechanistic changes that underlie life history variation of plethodontids and other salamanders.