Gene duplication is an important process in the functional divergence of genes and genomes. Several processes have been described that lead to duplicate gene retention over different timescales after both smaller-scale events and whole-genome duplication, including neofunctionalization, subfunctionalization, and dosage balance. Two common modes of duplicate gene loss include nonfunctionalization and loss due to population dynamics (failed fixation). Previous work has characterized expectations of duplicate gene retention under the neofunctionalization and subfunctionalization models. Here, that work is extended to dosage balance using simulations. A general model for duplicate gene loss/retention is then presented that is capable of fitting expectations under the different models, is defined at t = 0, and decays to an orthologous asymptotic rate rather than zero, based upon a modified Weibull hazard function. The model in a maximum likelihood framework shows the property of identifiability, recovering the evolutionary mechanism and parameters of simulation. This model is also capable of recovering the evolutionary mechanism of simulation from data generated using an unrelated network population genetic model. Lastly, the general model is applied as part of a mixture model to recent gene duplicates from the Oikopleura dioica genome, suggesting that neofunctionalization may be an important process leading to duplicate gene retention in that organism.