We also prove that the loss of Txnip in NK cells increases their sensitivity to activation, stimulating the production of larger amounts of IFN-γ in Txnip−/− (KO) NK cells than in wild-type (WT) NK cells under Pam3CSK4, a TLR2/TLR1 agonist, treatment and bacterial infection conditions. The gene discussed is IFNG; the disease is bacterial infectious disease.