Cell fate specification is achieved through the combinatorial activity of transcriptional regulators, which activate the developmental program necessary to establish a cell’s identity. The zinc finger transcription factor Glass (Gl) acts as a key determinant to establish photoreceptor identity in the Drosophila eye imaginal disc. In gl mutants, eye progenitor cells exhibit certain aspects of early neuronal differentiation and begin to organize into ommatidial clusters, but these cells fail to express photoreceptor-specific genes and display abnormal axon projections into the brain. It is thought that Gl directs the transition from an unspecified neuron to a photoreceptor identity by activating numerous downstream target genes. To determine if Gl is sufficient to induce any or all aspects of photoreceptor development we generated a UAS-gl transgenic line and performed misexpression experiments in neuronal and non-neuronal cells. We show that Gl misexpression in neuroblasts is sufficient to induce ectopic expression of the photoreceptor-specific gene chaoptin (Chp) in the larval brain. We also show that Gl is sufficient to induce Chp in non-neuronal cells of the larval wing and leg imaginal discs and that the Gl-expressing cells are not converted to a neuronal identity. Furthermore, Gl misexpression in imaginal discs or abdominal cells leads to ectopic eye pigment in the adult. We have performed RNA-seq in order to identify which genes can be ectopically induced by Gl in neuronal and non-neuronal cells. We find that some predicted Gl targets, including PvuII-PstI homology 13 (Pph13) and Eye-enriched kainate receptor (Ekar), as well as cardinal (cd), which encodes a pigment biosynthetic enzyme, can be induced in both cell types, while others are induced only in either neuronal cells or non-neuronal cells. Surprisingly, we find that many genes predicted to be Gl targets because of the presence of Gl binding sites in their regulatory regions and the co-variation of their expression with Gl, such as lozenge (lz) and kin of irre (kirre), are not induced in either context. We are currently performing a promoter analysis of these genes in order to identify possible repressors of Gl function. Our misexpression data and RNA-seq analysis also suggest that Gl may promote cone cell and pigment cell specification in addition to photoreceptor identity. We are currently investigating this possibility using cell type-specific knockdown and rescue experiments. .