Reactivation renders consolidated memory labile again, and the ensuing temporary reconsolidation process is highly susceptible to mnemonic modification. Here, we show that memories in such an unstable state could be influenced by sheer behavioral means, bypassing the need for pharmacological intervention. Across several experiments using a "face-location association" paradigm in which participants experienced a "Learning - New-learning - Final-test" procedure, we demonstrate that reactivated memory traces were hampered when the new learning was strategically administered at between 0-min and 20-min delay. Using fMRI, we further advance our theoretical understanding that this lability can be mechanistically explained by the differential activation in the hippocampal-amygdala memory system implicated by the post-activation new-learning whereas the mnemonic intrusion caused by newly learned memories is efficaciously reconciled by the left inferior frontal gyrus.