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Feeding behavior, essential for survival, is precisely orchestrated by the intricate interplay of peripheral signals and central neuronal circuits. Hypothalamic neurons expressing proopiomelanocortin (Pomc) gene induce satiety to limit food intake. While the significance of POMC neurons is well-recognized, the genetic mechanisms that govern the expression of hypothalamic POMC are not fully understood. A previous study that traced the origin and maturation of arcuate POMC neurons in the developing and early postnatal hypothalamus, using single-cell RNA-seq transcriptomics on POMC-positive cells, revealed Six3 and Six6 are highly expressed in the canonical POMC neurons. This current study aims to elucidate the role of Six6 in relation to the early identification, expression, and regulation of hypothalamic Pomc expression. The results showed that embryonic deletion of Six6 significantly reduced Pomc expression, however, this reduction has not been observed in adult mice in which Six6 is deleted during adulthood. Deletion of Six6 in adult mice does not change Pomc expression in the pituitary. Further studies are needed to investigate whether there are any compensation mechanisms for Six6 function.