Notably, REDD1 preferentially interacts with newly synthesized free IκBα rather than with IκBα bound to the NF-κB p65/p50 dimer, inducing a delayed or sustained inflammatory response after LPS stimulation61 or stimulating low-grade inflammation under obesity-induced energy stress conditions6 (Fig. 2b). Here, NFKBIA is linked to obesity due to melanocortin 4 receptor deficiency.