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Unexpectedly, we found that knockout of the TF\n            <jats:italic>Klf2<\/jats:italic>\n            resulted in aberrant differentiation to exhausted-like CD8 T cells during acute infection. KLF2 was required to suppress the exhaustion-promoting TF TOX and to enable the TF TBET to drive effector differentiation. KLF2 was also necessary to maintain a polyfunctional tumor-specific progenitor state. 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