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Krüppel-like factors, (KLF)s are transcription factors that possess finger-like zinc structures binding to DNA; families of these transcription factors include 18 members that can bind to consensus DNA sequences, CACCC, and sites rich in GC sequences. KLFs can act as activators or repressors of gene transcription related to a wide variety of physiological processes including but not limited to cell cycle regulation, differentiation, and apoptosis. Thus, deregulation in these transcription factors is involved in pathologies such as endometrial, ovarian, colon, and metabolic diseases of the pancreas, liver, and heart muscle. To initiate these physiological and pathological events, members of KLFs interact with ligand-activated nuclear receptors such as Peroxisome Proliferator-Activated Receptor Gamma, (PPARγ) or PPAR; this has been observed in overexpression and activation of the PPAR receptor experiments. In previous studies, it was found that, compared to treatment with agonists from PPARγ, KLF6 is overexpressed in Caco-2 colon cancer cell lines. Therefore, the objective of this review article is to show the possible functional relationship that exists between different members of KLFs and PPARγ, in normal and pathological states.