Although our report does not show evidence that TLR2-regulated proinflammatory SASP signaling mediates lesion regression in LUAD (because these lesions cannot be tracked longitudinally), it is tempting to speculate that activated TLR2-SASP signaling in lung tumors instructs recruitment of macrophages to the epithelium to subsequently impair tumor progression via immune surveillance. The gene discussed is TLR2; the disease is neoplasm.