INS and cancer: The pathophysiological mechanisms associated with increased intramyocellular lipid deposits with cancer‐mediated weight loss are still not clear36; however, enhanced lipolysis, insulin resistance, and impaired mitochondrial oxidation are often implicated in the myosteatosis formation.6, 37, 38, 39 Notably, these phenomena are associated with enhanced inflammatory milieu,6, 39 suggesting that the individual inflammatory status may identify distinct myosteatosis pathophysiology that could modulate survival outcomes.