Necroptosis is a caspase-independent form of regulated cell death that is characterized by membrane permeabilization and rupture. This membrane rupture is responsible for the inflammatory properties of necroptosis and is critical for disease states involving this process. In efforts to understand how lipids might contribute to necroptosis, we previously showed that saturated very long chain fatty acids (VLCFAs) are functionally involved in this process, potentially through protein fatty acylation. Here we define the scope of protein acylation by saturated VLCFAs during necroptosis using a clickable lipid analog and IonStar quantitative proteomics.As a result, a total of 1672 proteins were quantified with high precision and no missing data across samples in the same condition. 1267 were detected with higher abundances in control cells and 405 were detected with higher abundance in necroptotic conditions.