AKT1 and Cachexia: Notably, the study by Park M-R et al. (2023) reported preserved villus and crypt architecture with intact tight junctions, yet profound functional impairment was evident, including remodeling of lacteal lymphatic endothelium from permeable “button-like” to impermeable “zipper-like” VE-cadherin junctions, VEGFR2/AKT hyperphosphorylation, sequestration of oversized chylomicrons (>600 nm) in trans-Golgi cisternae, impaired lipid absorption, delayed intestinal transit, and cachexia independent of anorexia [104].