Furthermore, subclinical impairment of natural killer cell function and other cytotoxic effector mechanisms associated with PRF1 p.Ala91Val heterozygosity may promote the release of pro-inflammatory cytokines, including TNF, IL-6, and IFN-γ [41,42], fostering a microenvironment conducive to tumor initiation and progression. The gene discussed is PRF1; the disease is neoplasm.