The cellular environment is organised by a network of membranes that compartmentalize the cell and protect organelles. These membranes, composed primarily of lipids and proteins, are dynamic and can respond rapidly to metabolic changes or stresses, even generating new membranes when required. Such alterations in membrane homeostasis rely on efficient lipid transport. The highly conserved ‘funnel-like’ VPS13 family of proteins are found positioned at contact sites between organellar membranes, where they siphon lipids from one membrane to another. Humans have four proteins encoding VPS13 family members; VPS13A, VPS13B, VPS13C and VPS13D. Remarkably, defects in each of these proteins leads to diverse neurodegenerative diseases, indicating that despite their common function in lipid transport, each family member fulfills a unique function that is required to maintain neuronal health in human. In this work, we compare the function of two of these family members in a neuroblastoma cell line; VPS13C, implicated in Parkinson’s disease and VPS13D, linked to spastic ataxia. Understanding the functional differences in these proteins can help elucidate the underlying mechanism of their pathologies.