“…The CRP turnover model predicted both the average and individual CRP concentrations under the steady-state assumption: only baseline IL-6, baseline TS, disease stage, and smoking status affected CRP production, i.e., for a non-smoker with stage IV NSCLC, baseline IL-6 of 2.57 pg/mL and TS of 8.25 cm (median values), K in was estimated to be 0.297 (mg•L −1 )•h −1 , corresponding to a population steady-state baseline CRP concentration of 8.14 mg/L (Table 2) [41]. Current smokers, with disease stage IV, high baseline IL-6 (14.9 pg/mL, i.e., 95th percentile), and high tumor load (baseline TS: 17.8 cm, i.e., 95th percentile) would have a 68.3-fold higher K in and consequently a less favorable higher inflammatory level compared to non-smokers with less aggressive disease stage (stage IIIB), lower baseline IL-6 (0.438 pg/mL, i.e., 5th percentile), and lower tumor load (baseline TS: 2.20 cm, i.e., 5th percentile).…”