Cellular stress responses are mediated through conserved signaling pathways that translate external and internal perturbations into adaptive molecular programs. Although the components of these pathways are well characterised, less attention has been given to the intrinsic limits of their signaling capacity. Existing models often assume a proportional relationship between stress intensity and signaling output; however, biochemical constraints suggest that stress signaling is subject to saturation. This paper proposes a conceptual framework in which cellular stress pathways exhibit finite signaling capacity, resulting in qualitative changes in cellular outcomes once saturation thresholds are exceeded. By synthesising evidence from receptor kinetics, signal transduction cascades, and transcriptional regulation, this model provides a systems-level explanation for why mild stress promotes adaptation, whereas excessive stress leads to dysregulation or cell death. This work is theoretical in nature and does not present original experimental data. The framework is intended to organise existing observations and guide future experimental investigation.