Dear editor, Despite the growing number of treatments approved for inflammatory bowel disease (IBD), patient outcomes can still be unsatisfactory due to highly variable response rates. 1 Vedolizumab, first alternative biological for antitumour necrosis factor (TNF) in IBD management, targets α4β7 integrin heterodimers on circulatory T cells and inhibits their binding to mucosal addressin cell adhesion molecule 1 (MAdCAM-1). Despite its excellent benefit-risk profile, only 40-60% of IBD patients will respond, emphasizing the need for personalized medicine. 1,2 We performed the largest real-life prospective multicentre cohort study reported to date (n = 71) with serial sample collection at week (w) 0, 2, 6, 10 (only for CD) and 14 (Figure 1), to evaluate whether integrin expression profiles on circulatory T cells are potential biomarkers of vedolizumab response. The definition of response is described in Table S1.Although vedolizumab only targets α4β7, other dimers contribute to lymphocyte infiltration in the gut mucosa of IBD patients, including α4β1 and αEβ7. 2,3 Therefore, a highly qualitative flow cytometry analysis of α4, αE, β1 and β7 (Supplementary methods and Figures S1-S4) was performed on peripheral blood mononuclear cells of 44 ulcerative colitis (UC) and 27 Crohn's disease (CD) patients with moderate-to-severe disease, who initiated vedolizumab as part of their conventional treatment plan (Table S2). Response rates at w14 were similar as previously reported (Table S3) 1,2 and were not linked with age, gender, age at diagnosis, baseline C-reactive protein (CRP) and previous anti-TNF use. The biochemical response rate was significantly higher in UC patients with left-sided colitis than in those with pancolitis (66.7% vs. 33.3%; p = .015), and similar trend could be observed in endoscopic responders (72.0% vs. 24.0%; p = .066), partially confirming the data of Scarozza et al. 4 Current or previous smoking was associated with clinical and endoscopic response in UC (p = .040 and p = .039, respectively) (Table 1).