Since the in vitro enforced expression of FLIP in myeloid cells promotes the overexpression of several pro-inflammatory cytokines (i.e., IL-6, IL-7, IL-10, CSF3, and TNF-α) by a “steered” NF-κB activation, which also results in enhanced STAT3-signaling activation [35], we argue that a pervasive inflammatory loop is established by FLIP through the joint action of NF-κB and STAT3 during CRS evolution. The gene discussed is TNF; the disease is congenital rubella syndrome.