The question is deliberately provocative. However, if we reflect on the data about the treatment with terlipressin and albumin of type 2 hepatorenal syndrome (HRS), we have to recognize that despite a good response rate, there is a frustrating rate of recurrence. 1 In addition, despite some anecdotal pioneering approaches, 2 terlipressin remains a drug for use only in inpatients where available. We, therefore, need to recognize that the only indication for treating type 2 HRS for a patient who is a candidate for liver transplantation (LT) is to improve posttransplant outcomes, 3,4 at least in those countries in which a specific prioritization policy for LT has been developed in relation to HRS and its treatment. 5 In patients with potentially reversible renal dysfunction, such as type 2 HRS, predicting whether there will be sufficient return of native kidney function is sometimes difficult. Nevertheless, it has been established that the phenotype of acute kidney injury (AKI) at the time of LT has a great impact on patient survival and renal outcomes after LT, 6,7 with both being worse at 1 and 5 years after LT for acute tubular necrosis (ATN) compared to those with HRS. At 5 years, the prevalence of chronic kidney disease (CKD; stage 4 or 5) was significantly higher in the ATN group compared to the HRS group (56% versus 16%; P < 0.001). 6 There is little information on the effects of treatment with vasoconstrictors plus albumin in patients with HRS awaiting LT on the outcomes after LT, either in terms of survival or renal outcomes.In this issue of Liver Transplantation, Rodriguez et al. 8 reports the effects of treatment of type 2 HRS in LT candidates. The most notable finding was that an increase in glomerular filtration rate (GFR) in patients who had type 2 HRS before LT did not offer any significant advantage after LT. Importantly, there were no significant differences between patients with or without reversal of type 2 HRS before LT in relation to the development of AKI, renal replacement therapy, a change in serum creatinine (sCr) or in estimated glomerular filtration rate (eGFR) over time, or to the development of CKD by 1 year after LT. 8 Before we discuss the potential reasons for this therapeutic failure, it should be pointed out that this retrospective study was performed at a single, very valuable center in Spain. This observation is important because, as highlighted by Rodriguez et al. 8 in the discussion, the study was performed under 2 conditions that reduced the time to LT for patients with type 2 HRS, namely, (1) a very high rate of organ donation and (2) as of 2007, a priority allocation system in the waiting list that used the maximum value of sCr reached in Model for End-Stage Liver Disease (MELD) score updates for patients with HRS, which was to avoid a reduction of MELD after HRS reversal. By reducing the waiting time for LT in patients with type 2 HRS regardless of whether they were treated or how they responded, this could have masked any