Psoriasis is a long-term chronic inflammatory condition primarily affecting the skin and is associated with significant morbidity that extends beyond the skin manifestations, like psoriatic arthritis. It is characterised by inflammation and altered epidermal differentiation, which leads to red lesional plaques and scaling in the skin. There is a need for more effective, specific, long-term, safe and sustainable treatment for psoriasis. The present project aimed to use the phosphorodiamidate morpholino (PMO) chemistry to develop antisense oligomer (ASO) based therapeutics for psoriasis vulgaris. In our previous studies, we described whole transcriptome profiles of the psoriatic skin, and based on these RNA profiles, we identified the transcripts that are upregulated explicitly during psoriasis. Our experiments aimed to disrupt the expression of IL36R, S100A8 and S100A9 by ASOs. Using PMO chemistry, we developed highly specific and functionally effective ASOs that block the inflammatory pathways that cause psoriasis. We designed and functionally validated PMO oligonucleotides to skip exons 9 and 10 of the IL36R gene. We also designed and validated PMO ASOs to block the translation of S100A8 and S100A9 genes. In my presentation, I will describe the design of PMOs, their essential characteristics, molecular effects, and efficiency in the cellular models of psoriasis. I also present the results from the functional studies indicating the feasibility and translational potential of PMO chemistry as genomic therapeutics for psoriasis. Finally, I will discuss the development details and further plans with PMO antisense for psoriasis from the perspective of genomic medicine.