In 1999, the journal JCI published a study by Michel Eichelbaum and colleagues showing that the absorption of orally administered digoxin is influenced by the level of intestinal P-glycoprotein (P-gp). Rifampin treatment significantly reduced digoxin plasma concentrations after oral administration and to a lesser extent after intravenous administration. Rifampin also increased intestinal P-gp levels by 3.5-fold, which correlated with the area under the plasma concentration curve (AUC) of digoxin up to 144 hours. The study concluded that intestinal P-gp affects digoxin bioavailability, and the reduced oral bioavailability during rifampin is due to P-gp induction. However, subsequent feedback from Chiou et al. raised two issues. First, data pairs in the study were transposed and misassigned, leading to revisions in Figure 2c and Table 3. The corrected data showed a slight decrease in the Spearman rank correlation from 0.78 to 0.71, but the main conclusions remained valid. Second, the calculation of oral digoxin bioavailability AUC was clarified. The study used AUC0-144h instead of AUC0-00 and AUCiv from the control period to calculate bioavailability during rifampin. Recalculating with the correct data showed a slight difference in bioavailability (49.5% vs. 44%), but the main findings and conclusions were not invalidated. The study highlights the role of intestinal P-gp in drug interactions and the importance of accurate data interpretation in pharmacokinetic research.In 1999, the journal JCI published a study by Michel Eichelbaum and colleagues showing that the absorption of orally administered digoxin is influenced by the level of intestinal P-glycoprotein (P-gp). Rifampin treatment significantly reduced digoxin plasma concentrations after oral administration and to a lesser extent after intravenous administration. Rifampin also increased intestinal P-gp levels by 3.5-fold, which correlated with the area under the plasma concentration curve (AUC) of digoxin up to 144 hours. The study concluded that intestinal P-gp affects digoxin bioavailability, and the reduced oral bioavailability during rifampin is due to P-gp induction. However, subsequent feedback from Chiou et al. raised two issues. First, data pairs in the study were transposed and misassigned, leading to revisions in Figure 2c and Table 3. The corrected data showed a slight decrease in the Spearman rank correlation from 0.78 to 0.71, but the main conclusions remained valid. Second, the calculation of oral digoxin bioavailability AUC was clarified. The study used AUC0-144h instead of AUC0-00 and AUCiv from the control period to calculate bioavailability during rifampin. Recalculating with the correct data showed a slight difference in bioavailability (49.5% vs. 44%), but the main findings and conclusions were not invalidated. The study highlights the role of intestinal P-gp in drug interactions and the importance of accurate data interpretation in pharmacokinetic research.