Distinct postoperative dynamics of sAXL and GAS‐6 with regard to the extent of liver resection as well as the fact that patients with LD and morbidity failed to increase on POD1 led us to hypothesize that patients with underlying liver disease might suffer from prior chronic and consequently exhaustive activation of AXL/GAS‐6 signaling, especially because patients with preoperatively elevated concentrations, as found in the context of CLD, were unable to respond with a further boost in the signaling activity after induction of liver regeneration. The gene discussed is AXL; the disease is liver disorder.