Psoriasis is a chronic inflammatory skin disease with a strong genetic predisposition and autoimmune traits. The global prevalence is about 2%, varying by region. Psoriasis vulgaris, or plaque-type psoriasis, is the most common form, characterized by erythematous, scaly plaques on the trunk and extensor surfaces of the limbs. Other clinical subtypes include inverse psoriasis, guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. Psoriasis is associated with comorbidities such as hyperlipidemia, hypertension, coronary artery disease, type 2 diabetes, and metabolic syndrome. Psoriatic arthritis, a common complication, involves joint involvement and nail changes. The pathogenesis of psoriasis involves sustained inflammation leading to uncontrolled keratinocyte proliferation and dysfunctional differentiation. Key inflammatory pathways include the TNFα–IL-23–Th17 axis, with IL-17A/F playing a crucial role. Genetic factors, including HLA-Cw6, PSORS1, and CARD14, contribute to disease susceptibility. Epigenetic mechanisms, such as lncRNA and miRNA expression, also play a role. The skin microbiome, including Malassezia and Staphylococcus, is altered in psoriatic plaques. Treatment options range from topical therapies to systemic treatments like methotrexate, cyclosporine, and retinoids. Biologics, including TNF-α inhibitors and IL-23/IL-17 inhibitors, have shown significant efficacy in managing psoriasis. Biosimilars are also being developed to address patent expirations.Psoriasis is a chronic inflammatory skin disease with a strong genetic predisposition and autoimmune traits. The global prevalence is about 2%, varying by region. Psoriasis vulgaris, or plaque-type psoriasis, is the most common form, characterized by erythematous, scaly plaques on the trunk and extensor surfaces of the limbs. Other clinical subtypes include inverse psoriasis, guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. Psoriasis is associated with comorbidities such as hyperlipidemia, hypertension, coronary artery disease, type 2 diabetes, and metabolic syndrome. Psoriatic arthritis, a common complication, involves joint involvement and nail changes. The pathogenesis of psoriasis involves sustained inflammation leading to uncontrolled keratinocyte proliferation and dysfunctional differentiation. Key inflammatory pathways include the TNFα–IL-23–Th17 axis, with IL-17A/F playing a crucial role. Genetic factors, including HLA-Cw6, PSORS1, and CARD14, contribute to disease susceptibility. Epigenetic mechanisms, such as lncRNA and miRNA expression, also play a role. The skin microbiome, including Malassezia and Staphylococcus, is altered in psoriatic plaques. Treatment options range from topical therapies to systemic treatments like methotrexate, cyclosporine, and retinoids. Biologics, including TNF-α inhibitors and IL-23/IL-17 inhibitors, have shown significant efficacy in managing psoriasis. Biosimilars are also being developed to address patent expirations.