Epigenetics relies in large part on histone modifications and the proteins which make and recognize these modifications. Chromatin readers are a family of proteins which recognize different histone modifications and coordinate the appropriate chromatin rearrangements. A subset of chromatin readers are chromodomain containing proteins that are thought to recognize methylated histone tails, though how they influence gene expression remains largely unknown. One such chromatin reader is encoded by the kismet (kis) gene in Drosophila melanogaster. Decreased kismet function leads to defects in axonal guidance and pruning in mature neurons. The Kismet protein shares homology with the mammalian Chromodomain Helicase DNA binding (CHD) subgroup III family of proteins, including CHD7, an ATP-dependent chromatin remodeling protein. Haploinsufficiency of the CHD7 gene leads to CHARGE syndrome, a congenital neurodevelopmental disorder that affects approximately 1 in 10,000 individuals worldwide. Here we show that axon pruning defects are present in both kis mutants and flies expressing RNAi mediated knockdown of kismet. Further, we show the pruning defects are due to a decrease in expression of the steroid hormone receptor Ecdysone Receptor isoform B1 (EcR-B1) in the mushroom body Kenyon cells. Supplementing with exogenous EcR-B1 rescues pruning defects in two kis mutant backgrounds. Additionally, knocking down kismet leads to a global decrease in H3K4me3, a histone modification associated with actively transcribed chromatin. Elucidating the mechanism of Kismet-mediated EcR-B1 expression will provided greater insight into the epigenetic regulation of neuronal gene expression in general, and will be crucial to further the understanding of neurodevelopmental events that lead to CHARGE syndrome. .