Stress resilience, an individual’s ability to recover from or to maintain normal activities despite stressor exposure, is critical for fitness and in many cases relates to HPA flexibility or the rapid reversible plasticity in HPA axis function. A co-chaperone molecule involved in glucocorticoid receptor activity, FKBP5, may mediate HPA flexibility and stress resilience because it affects how individuals can regulate glucocorticoids (GCs) and capacitate their ability to adjust phenotypes appropriately to adverse conditions. Although well-studied in the biomedical field, FKBP5 research on wild vertebrates is limited. Here, we asked about the role of FKBP5 in coping with adversity in a wild species. We exposed house sparrows (Passer domesticus) to 20 days of a chronic stress protocol, while others were only exposed to daily husbandry. At capture and after the chronic stress protocol, we measured baseline, stress induced, and negative feedback levels of GCs. In the blood, we measured FKBP5 expression and GC level at both time points. At the end of the experiment, we measured FKBP5 expression in the hippocampus and hypothalamus. We hypothesized that FKBP5 expression in the blood would correlate with expression in these tissues. We expected that FKBP5 expression would increase in response to acute stress but more so to chronic stress. We also hypothesized that individuals which had a smaller increase in FKBP5 expression would have higher HPA flexibility allowing them to adjust their GC response to the current conditions. We supposed that individuals with higher HPA flexibility would cope better with current conditions suggesting higher stress resilience and that FKBP5 is a key mediator of HPA axis flexibility.