Fibroblast growth factor 16 (FGF16) is preferentially expressed in the heart after birth, suggesting its regulation is associated with tissue-specific chromatin remodeling and DNA-protein interactions. Mutation of the MEF2 site resulted in a blunting of FGF16 promoter activity in transfected neonatal rat cardiac myocytes, that chromatin remodeling and MEF2 binding in the FGF16 promoter contribute to expression in the postnatal heart. FGF16 involvement in the fine tuning of the human skeleton of the hand. Impaired FGF16 function may also be responsible for connective tissue symptoms in MF4 patients. FGF16 expression is markedly increased in ovarian tumors, and FGF16 in conjunction with Wnt pathway contributes to the cancer phenotype of ovarian cells and suggests that modulation of its expression in ovarian cells might be a promising therapeutic strategy for the treatment of invasive ovarian cancers.