The discovery of BRUCE as a multifunctional MASH suppressor represents a paradigm shift in understanding disease progression, as it uniquely integrates three fundamental protective mechanisms: (1) mitochondrial metabolism regulation (maintaining FAO and ATP production to prevent steatosis and oxidative stress); (2) genomic stability maintenance (repairing oxidative DNA damage); and (3) cell viability (blocking apoptosis and cell death-induced release of pro-inflammatory Damage-Associated Molecular Patterns (DAMPs)). Here, BIRC6 is linked to steatosis.