A core pathogenic feature of PCM is a self-perpetuating circuit: ductal ectasia-generated DAMPs activate PRRs, including TLR4 and NLRP3, triggering NF-κB signaling to induce the release of pro-inflammatory cytokines IL-1β and IL-6 and the upregulation of adhesion molecules ICAM-1. The gene discussed is NFKB1; the disease is paracoccidioidomycosis.