Abstract: Parkinson’s disease (PD), a prevalent neurodegenerative disorder, is characterized by the loss of dopaminergic neurons and the aggregation of α-synuclein protein into Lewy bodies. While the current standards of therapy have been successful in providing some symptom relief, they fail to address the underlying pathophysiology of PD and as a result, they have no effect on disease progression. They also carry the risk of unacceptable side effects that can impair quality of life. Fortunately, recent research has pointed towards Fas apoptosis inhibitory molecule (FAIM) as a less problematic and potentially disease modifying target for new therapies given the newfound evidence of a possible link between FAIM, PD pathogenesis, and α-synuclein aggregation. This perspective seeks to elucidate this relationship and its implications for future research and treatment modalities.