NFKB1 and Insulin resistance: This contributes to adipose tissue dysfunction, whereas WAT inflammation and oxidative stress supervene, promoting the release of pro-inflammatory adipokines, leptin and adiponectin, along with enormous levels of cytokines (IL-6, IL-1b, TNF-α) and NF-κB activation, all ending in a cycle of sustained systemic insulin-resistant state [36,98,99,100].