Background: Signal transducer and activator of transcription (STAT) proteins play key roles in development, growth, and homeostasis. These roles have principally been assigned to their “canonical” function as inducible transcriptional activators acting downstream of cytokines and other factors. However, variant “non-canonical” functions have also been identified. The potential in vivo role for non-canonical STAT functions was investigated in the zebrafish model. Methods: Two zebrafish Stat5.1 mutants were generated using CRISPR/Cas9 that should impact canonical functionality: one with a deleted transactivation domain (\mathrm{\Delta }TAD) and another with a disrupted tyrosine motif (\mathrm{\Delta }TM). Immune cell development, growth, and adiposity of these Stat5.1 mutants were assessed in comparison to a Stat5.1 knockout (KO) mutant in which both canonical and non-canonical functions were ablated. Results: Both the \mathrm{\Delta }TAD and \mathrm{\Delta }TM mutants showed significantly reduced embryonic T lymphopoiesis, similar to the KO mutant. Additionally, adult \mathrm{\Delta }TAD and \mathrm{\Delta }TM mutants displayed a decrease in T cell markers in the kidney, but not as severe as the KO, which also showed T cell disruption in the spleen. Severe growth deficiency and increased adiposity were observed in all mutants, but \mathrm{\Delta }TAD showed a more modest growth defect whereas \mathrm{\Delta }TM exhibited more profound impacts on both growth and adiposity, suggesting additional gain-of-function activity. Conclusions: These results indicate that canonical Stat5.1 plays a major role in T cell development and growth throughout the lifespan and non-canonical Stat5.1 functions also contribute to aspects of adult T lymphocyte development and growth, with alternate functions impacting growth and adiposity.