Interactions between the brain networks and subnetworks are crucial for active and resting cognitive states. Whether a subnetwork can restore the adequate function of the parent network whenever a disease state affects the parent network is unclear. Investigations suggest that the control of the anterior insula-based network (AIN) over the default-mode network (DMN) and central-executive network (CEN) is decreased in individuals with mild cognitive impairment (MCI). Here, we hypothesized that the posterior insula-based network (PIN) attempts to compensate for this decrease. To test this, we compared a group of MCI and normal cognitive individuals. A dynamical causal modeling method has been employed to investigate the dynamic network controls/modulations. We used the resting state functional MRI data, and assessed the interactions of the AIN and of the PIN, respectively, over the DMN and CEN. We found that the greater control of AIN than that of DMN (Wilcoxon rank sum: Z = 1.987; p = 0.047) and CEN (Z = 3.076; p = 0.002) in normal group and the lower (impaired) control of AIN than that of CEN (Z = 8.602; p = 7.816 × 10-18). We further revealed that the PIN control was significantly higher than that of DMN (Z = 6.608; p = 3.888 × 10-11) and CEN (Z = 6.429; p = 1.278 × 10-10) in MCI group where the AIN was impaired, but that control was significantly lower than of DMN (Z = 5.285; p = 1.254 × 10-7) and CEN (Z = 5.404; p = 6.513 × 10-8) in normal group. Finally, the global cognitive test score assessed using Montreal cognitive assessment and the network modulations were correlated (Spearman’s correlation: r = 0.47; p = 3.76 × 10-5 and r = -0.43; p = 1.97 × 10-4). These findings might suggest the flexible functional profiles of AIN and PIN in normal aging and MCI.