The study investigates the survival and recovery of Neuro-2a (N2a) cells following a cryogenic storage failure that exposed them to extreme stress conditions, such as hypoxia, hypothermia, and acute toxicity. Remarkably, a small fraction of the cells survived and eventually recovered. To understand the underlying resilience mechanisms, we created a model to replicate the dewar failure event and examined changes in phenotype, transcriptomics, proteomics, and mitochondrial activity of the surviving cells during recovery. The results revealed that the surviving cells initially displayed a stressed morphology, with irregular membranes and clustering. They showed increased expression of proteins related to DNA repair and chromatin modification pathways, as well as heightened mitochondrial function, shortly after the stress event. As recovery progressed, these stress-responsive pathways and mitochondrial activity normalized, indicating a return to a stable state. These findings suggest that an initial robust energetic state supports key stress-responsive pathways, facilitating cell survival and recovery after extreme stress. This work provides valuable insights into cellular resilience mechanisms, with potential implications for improving cell preservation and recovery in biomedical applications and developing therapeutic strategies for conditions involving cell damage and stress.