Gait dysfunction is a key defining feature of Parkinson’s disease (PD), and is associated with symptoms of freezing and an increased risk of falls. In this narrative review, we cover the putative mechanisms of gait dysfunction in PD, the assessment of gait abnormalities, and the management of symptoms caused by the inherent difficulty in walking. Our understanding of the causes of gait problems in PD has progressed in recent times, moving from neurocognitive theory to correlates of affected neuronal pathways. In particular, this can be shown to correspond with abnormalities in responses to dual-task paradigms and dysfunction in cholinergic signaling. Great progress has been made in the sophistication and precision of gait assessment; however, it has firmly remained in the research domain. There is significant momentum behind wearable technologies that can be used by patients in their own environment, acting as digital biomarkers that can not only reflect progression but also independently discriminate PD from non-PD individuals. The treatment of gait dysfunction has historically relied on physical therapies and training combined with a view to mitigating the impact of such consequences as falls. Pharmacological therapies that are the mainstay of treatment in PD have tended to address symptoms like bradykinesia; however, optimization of dopaminergic therapies likely has a positive effect on quality of gait. Other targets have been assessed with the goal of improving gait, of which medications that improve cholinergic signaling appear most promising. Neuromodulation techniques are increasingly used in the form of deep-brain stimulation; however, standard targets, such as the globus pallidus interna, have a modest effect on gait. Considerable benefit has been seen through targeting the pedunculopontine nucleus, and a dual-target approach may be warranted. Stimulation of the spinal cord and brain through direct or magnetic approaches has been assessed, but requires further evidence.