Firstly, while QRICH1 is proposed to interact with ATF6 as a transcriptional regulator, it may interact with other stress-responsive pathways such as NF-κB-mediated inflammation, JNK/p38 MAPK signaling, or oxidative stress pathways, all of which have been implicated in cardiac hypertrophy and remodeling. This evidence concerns the gene MAPK8 and cardiac hypertrophy.