The pathogenesis can be divided into five distinct phases [41]: sebaceous glands secrete lipids onto the skin surface; Malassezia colonizes areas covered with lipids; Malassezia secretes lipase, which produces free fatty acids and lipid peroxides that activate the inflammatory response; the immune system produces cytokines such as IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10 IL-12, and TNF-α, which stimulate keratinocyte proliferation and differentiation; and disruption of the skin barrier, leading to clinically evident erythema, pruritus, and scaling. The gene discussed is IL1B; the disease is Erythema.