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We would like to thank Drs Yu, Wang, Huang and Chen for their comments [1] on our article [2] exploring the link between growth differentiation factor-15 (GDF-15), liver disease-driving pathomechanisms and liver-related outcomes in patients with cirrhosis. We fully agree with our colleagues that GDF-15 appears to be a key biomarker reflecting multiple drivers of liver disease progression, including bacterial translocation, systemic inflammation and fibrogenesis—consistent with the known role of this cell stress–induced cytokine in other chronic diseases [3]. With regard to the stated considerations, we first want to address the comments concerning the clinical utility of the proposed GDF-15 cut-off and our statistical approach. We agree that recruitment from a specialised hepatic haemodynamic lab at a tertiary care centre, together with exclusion criteria implemented to reduce confounding, may limit the generalisability of this cut-off to broader cirrhosis populations. However, we would like to emphasise the hypothesis-generating and exploratory nature of our work, which aimed to demonstrate that elevated GDF-15 levels reflect not only fibrogenesis and inflammation but also the risk of disease progression—specifically in cirrhosis. Accordingly, using maximally selected rank statistics, we sought to identify the most precise cut-off within our specific cohort to further illustrate the significantly increased risk of hepatic decompensation and death in patients with higher GDF-15 levels. Further studies and external validation are needed to determine the optimal GDF-15 threshold for risk stratification—considering distinct aetiologies and stages of liver disease—prior to potential clinical implementation. Furthermore, we want to emphasise that a central finding of our study was the prognostic value of GDF-15 when analysed as a continuous variable—thus avoiding dichotomisation and the associated risk of losing information. Specifically, higher GDF-15 levels were found to remain significantly linked to a higher risk of disease progression in multivariable models accounting for established liver disease drivers. While we acknowledge that some covariates included in the multivariable models are associated with overall liver disease severity and may therefore share information, variance inflation factor analysis did not indicate relevant multicollinearity. Regarding the second comment on the timing of GDF-15 measurements, we agree that serial assessments may provide additional clinical value and could potentially guide decision-making during the course of liver disease. This is particularly relevant in the light of growing evidence demonstrating the prognostic importance of, among others, longitudinal changes in liver stiffness [4] and laboratory markers reflecting hepatic function [5]. Thus, future investigations on the longitudinal trajectories of GDF-15 over the course of liver disease and assessment of their independent prognostic value for clinical events—on top of established markers of synthetic dysfunction, fibrogenesis and systemic inflammation—are warranted. In conclusion, we appreciate the thoughtful considerations raised by our colleagues and share the view that GDF-15 represents a promising biomarker in cirrhosis, reflecting key disease-driving pathomechanisms while providing independent prognostic information. Further studies are warranted to validate our findings, define optimal cut-off points for clinical risk stratification and clarify the precise pathophysiological processes underlying the role of GDF-15. Benedikt Silvester Hofer: writing – original draft, writing – review and editing. Thomas Reiberger: writing – review and editing, supervision. Thomas Gremmel: writing – review and editing, supervision. The authors have nothing to report. B.S.H. received travel support from Ipsen and Falk, speaking honoraria from Gilead and honoraria for educational materials from Ipsen. T.R. received grant support from Abbvie, Boehringer Ingelheim, Gilead, Intercept/Advanz Pharma, MSD, Myr Pharmaceuticals, Philips Healthcare, Pliant, Siemens and W. L. Gore & Associates, speaking honoraria from Abbvie, Echosens, Gilead, Intercept/Advanz Pharma, Roche, MSD, W. L. Gore & Associates, consulting/advisory board fee from Abbvie, Astra Zeneca, Bayer, Boehringer Ingelheim, Gilead, Intercept/Advanz Pharma, MSD, Resolution Therapeutics, Siemens; and travel support from Abbvie, Boehringer Ingelheim, Dr. Falk Pharma, Gilead and Roche. T.G. received speaker fees from Amgen, Bayer, Boehringer-Ingelheim, Bristol Myers Squibb, Daiichi-Sankyo, Novartis and Pfizer, and grant support from Boehringer-Ingelheim, Bristol Myers Squibb, Medtronic and Abbott. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.