Th17 cells are key players of the adaptive immune system. They mainly take part in responses to extracellular parasites and neutrophil recruitment. They can infiltrate into the inflammation sites and survive for long periods of time. Their malfunction leads to the manifestation of several autoimmune diseases, such as Multiple Sclerosis and Rheumatoid Arthritis. The main reason behind their roles in autoimmune pathogenicity is thought to be their longevity and resistance to apoptosis. One of the main players of apoptosis, Fas, has been found to have non-apoptotic roles and is a candidate for the survival mechanisms of Th17 cells. This study aims to discover possible non-apoptotic roles of the Fas signaling pathway in Th17 cell functions. For this purpose, buffy coats of healthy individuals were used to isolate PBMCs and CD4+CD45RA+ naive T cells were sorted from the PBMCs. Obtained naive T cells were cultured under Th17 polarizing conditions and the expressions of Fas, FasL, TNFR1, and TNF-α have been monitored along with apoptosis. The expression of Fas has been found to significantly increase in the cells cultured under Th17 polarizing conditions. However, there were no FasL and TNFR1 expressions observed. The expression of TNF-α was observed on both the negative culture and Th17 polarizing culture, however, there was no significant difference found. In addition, there was no increase in apoptosis in neither culture. In summary, Fas expression has been found to increase in the cells cultured under Th17 polarizing conditions. Further investigation of possible survival mechanisms, such as NFkB, in these cells can shed light on the effects of the Fas signaling pathway on the longevity of Th17 cells.