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We thank Drs Saluja and Chinnaratha, and Drs Lu and Ding for their interest and comments on our randomised trial [1-3]. The authors of both of these letters raise some important concerns about sample size calculation. While some of the comments are justified, the authors had to make the best with the data available before the RCT to inform the sample size calculation. There were no direct data to inform the sample size for the RCT which we had planned. There have been arguments against routine (mis)use of sample size calculations because of the unreliable nature of effect size which are often not available, and if available, may not be directly applicable to the planned trials or the settings. On the other hand, ‘trialist cops’ argue that underpowered studies are unethical. However, in context of our RCT, the concern is not valid. While our study was designed with a 10% non-inferiority margin, the short-taper arm (6 weeks) failed to meet this threshold. In fact, the data demonstrated a statistically significant advantage for the long-taper arm (10 weeks) in achieving the primary endpoint of steroid-free clinical remission at 6 months. This robust separation suggests that, in the context of our study's maintenance backbone, the 6-week taper is clinically insufficient for a significant proportion of patients. While it is easy, in retrospect, for the authors of the letters to provide a posthoc power calculation, alas, we were not privy to outcome of the study while planning the trial. An important argument could be if a longer taper provides a durable benefit or merely postpones relapse. Our data showed that while cumulative relapse rates at 6 months were numerically similar, the median time to relapse was significantly shorter in the short-taper arm (2 months) compared to the long-taper arm (5 months). In many clinical settings, particularly in low-to-middle-income countries (LMICs), thiopurines remain the primary steroid-sparing agents. Given their slow onset of action (typically 8–12 weeks), a 10-week steroid taper serves as an essential therapeutic bridge [3]. Shorter tapers may ‘unmask’ disease activity before the maintenance therapy has reached peak efficacy, leading to the early relapses observed in our short-taper cohort [4]. We agree that the ‘therapeutic context’ is shifting. In centres where biologics or small molecules are used upfront, the rapid onset of these agents may indeed allow for more aggressive steroid withdrawal [4, 5]. However, for the global majority of patients managed with 5-ASA and thiopurines, our findings provide a pragmatic evidence base for a more cautious 10-week approach to optimise long-term remission. While ‘steroid stewardship’ is vital to minimise adverse effects, our trial suggests that tapering too rapidly can compromise the durability of the initial response. In fact, a faster steroid taper, based on the evidence from our trial, is a recipe for failure of steroid therapy and, in principle, against ‘steroid stewardship’. We welcome further research evaluating whether modern, rapid-acting induction therapies can finally make shorter steroid tapers a safe and effective reality for all patients. ‘The authors’ declarations of personal and financial interests are unchanged from those in the original article [3]. V.S. wrote and all authors read and approved this letter. The authors have nothing to report. The authors declare no Conflicts of Interest. This article is linked to Kumar et al. papers. To view these articles, visit https://doi.org/10.1111/apt.70622, https://doi.org/10.1111/apt.70633 and https://doi.org/10.1111/apt.70509. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.