In line with this, upregulation of activating receptors NKG2D and CD8 was observed on CD56bright NK cells as well as downregulation of the inhibitory receptor NKG2A after tumor resection in non-adjuvant-treated CC patients, suggesting that both CD56dim NK and CD56bright NK cells acquired a more active phenotype after tumor resection and, therefore, possibly recovered from TME-induced immunosuppression. The gene discussed is KLRC1; the disease is neoplasm.