Microglia, the immune cells of the CNS, are crucial for the maintenance of homeostasis and the response to pathological challenges. Their activation profile is highly complex and layered. In the past decade, ferroptosis, an iron-dependent type of cell death, has been linked to neurodegeneration and therefore to microglia. Ferroptosis is the link between iron and lipid metabolism. The latter has been investigated in microglia due to its high relevance in neurodegenerative diseases. This report aims at providing insight into the influence of iron and lipid homeostasis on one another, as well as elucidating the role of fatty acid-binding protein 3 (FABP3) in this context. For this purpose, microglia were treated with lipids cholesterol rich from adult bovine serum, iron (III) citrate hydrate and a combination of the two. Gene expression and protein levels of ferroptosisrelated genes were assessed by qPCR and western blot respectively. Lipid droplets were stained with BODIPY 493/503 and then visualized by confocal microscopy. Experiments were repeated on a FABP3 KO cell line, generated with CRISPR-Cas9 gene editing. The findings highlight the association between cholesterol and iron metabolism, particularly their coupled effect on gene and protein regulation. In addition, they shed light on the function of FABP3 in microglia activation, which needs to be further explored to fully understand its potential as a biomarker for neurodegeneration.