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The education or licensing process is essentially required for the proper anti-tumor function of natural killer (NK) cells. Although several models for education have been proposed, the genetic factors regulating these processes still remain largely elusive. Here we show that FAM13A (family with sequence similarity 13, member A), strongly linked to the risk of prominent death-causing lung diseases, ie, lung cancer and chronic obstructive pulmonary disease, critically modulated NK cell maturation and effector functions. Fam13a depletion promoted NK cell maturation, KLRG1 (killer cell lectin-like receptor G1) expression in NK cells and NK terminal differentiation in homeostatic mice. NK cells from Fam13a-deficient mice had impaired IFN-γ production and degranulation. Strikingly, the number of lung metastases induced by B16F10 melanoma cells was increased in Fam13a-deficient mice. Collectively, our data reveal a pivotal role of FAM13A in slowing down NK maturation, but promoting NK cell effector functions and immune protection against tumor metastasis.