TRPV1 and congenital rubella syndrome: 2007), highlighting distinct pathophysiological mechanisms between stress‐induced and nerve‐injury‐induced pain hypersensitivity. Conversely, dynamic cold stimuli (e.g., acetone evaporation) are robustly enhanced by CRS (Bardin et al. 2009) and engage a central–peripheral interplay involving TRPV1‐dependent substance P release from TRPM8+ sensory neurons (F. Li et al. 2019).