There is a need for a system that can efficiently study transcription factor contribution and influence on retinal neuron fate. A tet-inducible CRISPR activation (CRISPRa) system was designed and cloned for dCas9, dCas12, and dCasMini to overexpress the transcription factor NEUROG2 and ASCL1, and subsequently transfected and integrated into induced pluripotent stem cells (iPSCs) for differentiation into retinal neurons. Using fluorescent imaging, we observed mosaicism of mRuby expression in the dCasMini-VPR cell line, which we hypothesize is due to epigenetic silencing at the AAVS1 safe harbor site, leading to poor differentiation of neurons after transfecting NEUROG2 gRNAs. Subsequently, we designed piggyBac-dCas-VPR transposon and saw better persistence of mRuby signal in vitro, indicating a promising alternative to gene-editing in traditional safe harbor loci. This study not only advances our understanding of CRISPRa in neuronal differentiation but also provides valuable insights for refining protocols in generating retinal ganglion cells, thereby contributing to potential therapeutic interventions for vision-related disorders.