Purpose: To determine whether B1 inhomogeneity-corrected volumetric T1 maps of gadoxetic acid-enhanced liver magnetic resonance (MR) imaging are able to demonstrate global liver function and functional heterogeneity in patients with cirrhosis and to investigate their relationship with the development of hepatic insuffciency and decompensation. Materials and Methods: This institutional review board-approved retrospective study with waiver of informed consent included 234 consecutive patients who underwent gadoxetic acid-enhanced liver MR imaging, including B1 inhomogeneity-corrected volumetric T1 mapping. For all patients, T1 relaxation times of the liver and liver volumes were measured on T1 maps. Liver T1 and functional liver volume-to-weight ratio (liver volume divided by liver T1 and the patient's weight) were compared between Child-Pugh class A and class B cirrhosis. Associations between serum markers, MR parameters, hepatic insuffciency, and decompensation were investigated by using Cox proportional hazards analysis. Results: Patients with Child-Pugh class B disease showed signifcantly longer liver T1 (548.2 msec ± 257.7 vs 372.2 msec ± 77.5, P <.0001) and lower kurtosis of liver T1 (29.1 ± 39.6 vs 43.9 ± 64.9, P =.016) than patients with ChildPugh class A disease. Prolonged liver T1 (≥462 msec) (hazard ratio [HR], 5.9; 95% confdence interval [CI]: 1.1, 62.8) and an albumin level of less than 3.5 g/dL (HR, 20.7; 95% CI: 3.9, 221.9) were independently associated with the development of hepatic insuffciency. Functional liver volume-to-weight ratio was associated with the development of hepatic decompensation in patients with ChildPugh class A disease (HR, 0.03; 95% CI: 0.004, 0.23). Conclusion: B1 inhomogeneity-corrected volumetric T1 mapping provided information on global liver function and demonstrated functional heterogeneity. In addition, prolonged liver T1 (≥462 msec) was associated with the development of hepatic insuffciency, and functional liver volume-to-weight ratio was negatively related with the development of decompensation in compensated cirrhosis.