CAR T therapy is a widely growing immunotherapy used to treat a range of cancers. However, a major issue that arises is a lack of persistence and a decrease in their effector potential. TCF1 is a transcription factor known to be vital in T cell development and differentiation and its expression correlates with increased T cell persistence in clinical settings. Given 𝛽-catenin is a coactivator of TCF1, its role has also been studied in improving persistence. Previous studies have shown that constitutive overexpression of a 𝛽-catenin-TCF1 fusion protein (TCF1fusion) increases the surface memory phenotype but is unable to increase CAR T persistence and may negatively impact the anti-tumor function seen when CAR T cells are challenged with tumor. In this study, we designed a drug-regulatable version of TCF1fusion to see if transient TCF1fusion expression can promote persistence and rescue an effector phenotype, as studied via a Nalm6-CAR T and 143b-CAR T co-culture. Co-culture data showed that brief expression of TCF1fusion prior to stimulation increases expression of memory markers and rescues effector function. These data highlight the importance of duration of TCF1fusion expression providing a promising launch point for future investigations.