The human brain is an incredibly complex machine. Mother nature has evolved to efficiently create such an intricate structure by massively overproducing neurons and synapses during human development. Over time, only half of these original neurons survive. How does the brain achieve this? How does it differentiate between those neurons that survive, and those that die? Current science has determined that the mechanisms of apoptosis and axon pruning are critical for the refinement of the developing brain. These processes are regulated by the balance of constructive cues, such as secretion of nerve growth factor, and regressive cues, such as the activation of death receptors. Death Receptor 6 (DR6) is a member of a receptor family identified to play a crucial role in nervous system development. The aim of our research is to study the effects of DR6 on the complexity of neurons in the sympathetic nervous system. Through examination of primary cultures from DR6 -/- and WT neurons by Sholl analysis, we find that DR6 has no significant effect on neurite complexity or axon growth cone size. Broadening our understanding of DR6’s role in the structure of the sympathetic nervous system could catalyze advancements in medicine connected to diseases that affect these developmental pathways. Eventually, this type of research has the potential to impact treatments for neurodegenerative disorders such as Charcot-Marie Tooth’s Disease and Alzheimer’s Disease. Understanding these complex processes that shape the nervous system’s circuitry is a critical first step in aiding the millions afflicted with these diseases.