Alzheimer’s disease affects a large portion of the population. Cell death research is vital for neurodegenerative diseases. Among the many types, ferroptosis is receiving increased attention. It is a programmed, iron-dependent cell death mechanism (Jiang, et al., 2021). It can be triggered by inhibiting the Xc- transporter, an antiporter (Ratan, 2020). Inhibiting this transporter leads to an accumulation of intracellular glutamate, leading to ferroptosis (He, et al., 2013). In the current study, ferroptosis was examined in HT22 cells, which are mouse hippocampal cells. This cell line is frequently used in glutamate toxicity studies because they are sensitive to glutamate-induced ferroptosis (He, et al., 2013). Thiamine is a vitamin required for cells to synthesize energy (ATP) (Panoff, 2021). Our hypothesis is that by increasing the amount of thiamine in the HT22 cells, the synthesis of energy will increase. I obtained negative results from my experiment last year when I used UK5099, a pyruvate transport inhibitor. The experiment setup from last year stayed the same, thiamine was just substituted for UK5099. Thiamine protecting HT22 cells from ferroptosis could offer insights into its protective mechanisms. Thiamine has not been tested on ferroptosis in neuroblasts. I found that thiamine did protect against ferroptosis. The protection was confirmed using MTT assays. Limitations included the duration of the experiment, the number of cells used, and the possibility that thiamine blocks erastin’s ability to block the Xc- transporter. These could limit the generalizability of the results but will be taken into account in the future.