In interphase, the genome is known to organize into topologically associated domains (TADs) of transcriptionally active and inactive gene clusters. Gene expression during this phase is dynamic and chromatin must reflect structural organization but maintain a level of plasticity in order to respond to different stimuli through gene expression changes. Stimuli like stressors can globally change the chromatin landscape in very short time scales. One such stressor is heat stress which can lead to reorganization of topologically associated domains in cultured insect cells. Interestingly, heat shock results in an increase of chromatin bound structural proteins and changes in TAD arrangements. However CAP-H2, a subunit of condensin II and regulator of genomic topology, levels are reduced on chromatin after heat shock. This contradictory result presents many questions such as what the role of CAP-H2 and therefore condensin II is during heat shock and what the fate of CAP-H2 is during this time. Investigation into the turnover of CAP-H2 using cell fractionation and western blots revealed that CAP-H2 is degraded after release from chromatin due to heat stress. Recovery after heat stress does not require CAP-H2 as knockdown with RNAi does not indicate significant levels of cell death compared to the control. Despite these results many questions still remain such as what the role CAP-H2 in re-establishing or restructuring of chromatin is during recovery? We hypothesize that condensin II may prevent long range interactions necessary during heat shock and facilitate short range interactions as cells recover.