EIF2A and colitis: In 19 core-DEGs, in addition to the above crosstalk molecules common to ER stress and ferroptosis, deletion of Bp65 (RELA) was found to significantly up-regulate ferroptosis and exacerbate colitis in IEC-specific NF-kappa Bp65 deficient mice, and phosphorylated Bp65 significantly inhibited ER stress by binding eIF2α [25].