Opening of chromatin by modification of histone tails is an important process in the synthesis of fungal secondary metabolites (SM). Trimethylation of histone H3 lysine 9 (H3K9me3) and occupancy of heterochromation protein-1(HepA) at this modification site are important marks of transcriptionally silent heterochromatin. In this work we investigate the role de-methylation of H3K9me3 plays in regulating secondary metabolism in Aspergillus nidulans. Our Chromatin Immunoprecipitation (ChIP) data provides evidence that both putative Jumonji C-family de-methylases present in the genome are involved in removing the methylation mark from H3K9me3. Deletion of one of the two genes repressed sterigmatocystin (ST) production and the expression of aflR, the main regulator of the ST gene cluster. Surprisingly, deletion of both de-methylases restored aflR gene expression, but not ST production. Metabolic and transcriptome analysis of the de-methylase mutants suggest that restoration of aflR expression is a consequence of de-regulation of primary metabolism, mainly affecting carbon utilization. ST production itself was not restored due to perturbations in primary metabolism presumably affecting precursor provision. Both, de-methylases and LaeA, the conserved global regulator of secondary metabolism, are required to replace the repressing methylation marks on H3 by activating marks.. These results are the first to provide evidence about the role of histone de-methylases in chromatin remodeling, primary metabolism, and secondary metabolism of A.nidulans.