**Theoretical and clinical implications** Overall, our findings provide evidence of partially distinct yet overlapping mechanisms underlying different stuttering behaviors, which has important theoretical implications for models of speech production and motor control. Specifically, these results support frameworks that differentiate between FB- and FF-based speech regulation, while also highlighting shared neural pathways. This view challenges the notion of a singular neural deficit in stuttering and instead points to a more nuanced, mechanism-specific perspective. Additionally, these findings motivate the need for theoretical models to account for individual variability in neural control strategies, which may inform more personalized approaches to understanding and treating stuttering. From a clinical standpoint, further research in this area has the potential to inform the development of more targeted behavioral and medical interventions for individuals who stutter, ultimately improving treatment efficacy and personalization. For example, if repetitions and prolongations are associated with an overreliance on auditory FB mechanisms, behavioral strategies targeting enhanced control of auditory feedback, such as those using speech feedback manipulation (e.g., delayed auditory feedback), could benefit individuals exhibiting these disfluency types. Similarly, if blocks are associated with difficulties in initiating speech due to disruptions in the FF system and subcortical timing mechanisms, treatment strategies focusing on enhanced speech initiation or smoother transitions between speech motor programs could be more effective for individuals who primarily exhibit blocks. Additional research could also inform future medical interventions (e.g., neuromodulation or pharmacological treatments) targeting specific neural pathways. Prior studies have reported increased fluency following stimulation to speech motor areas, including inferior frontal gyrus and supplementary motor area. Similarly, pharmacological interventions have targeted dopaminergic pathways, given the proposed role of dopamine dysregulation in stuttering. Building on these findings, individuals with FB-based disfluencies (e.g., repetitions, prolongations) may benefit from neuromodulation to the left vMC to right vPMC pathway, with the goal of recalibrating an overactive feedback system. For individuals with blocks, which may be linked to timing disruptions in subcortical circuits, pharmacological treatments targeting the basal ganglia or cerebellum could offer more tailored approaches to restore motor initiation and timing function. In conclusion, these findings underscore the potential for developing personalized, targeted interventions that consider the different neural mechanisms involved in various stuttering behaviors. By targeting the underlying neural mechanisms associated with different disfluency types, both behavioral and medical treatments for stuttering could be made more effective and personalized. Further research with larger sample sizes will provide stronger evidence to guide the development of future behavioral and medical interventions, helping to identify the most effective targets for treatment based on specific neural pathways associated with different disfluency types.