Cbl‐b deficiency prominently rescued the decreased IFN‐γ production and failed melanoma rejection observed in inactivated NK cells 119.In addition, genetic deletion of the Cbl‐b or targeted inactivation of its E3 ligase activity licensed NK cells to spontaneously reject melanoma metastasis through the ubiquitination of Tyro3, Axl, and Mer, which are members of TAM tyrosine kinase receptors. Here, AXL is linked to melanoma.