Specifically, peptides from P. acnes can bind to TLR2 on the membranes of keratinocytes and macrophages and then phosphorylate NF-κB, thus promoting the secretion of TNF-α, IL-1β, etc. These proinflammatory factors are responsible for the worsening of inflammation after the onset of acne resulting in hyperkeratosis with severe swelling, inflammatory infiltration, and granulomatous reaction [36]. The gene discussed is NFKB1; the disease is Hyperkeratosis.