TRIM63 and Cachexia: TNF-α, via TNFR1 and TNFR2 receptors, triggers the NF-κB signaling pathway [1,3] and promotes protein degradation via ubiquitin proteasome E3 ligases, specifically MurF1 and Atrogin1 [29], which are common in cancer patients and preclinical models of cachexia, where they facilitate the degradation of skeletal muscle proteins [30,31].