NLRX1 and neoplasm: Thanks to a newly characterized HPV16 E6/E7-expressing HNSCC mouse model (MOC2-E6/E7), syngeneic to C57BL/6, they also demonstrated that the CRISPR/Cas9-mediated depletion of NLRX1 in tumor cells could significantly increase STING activation upon poly(dA:dT) stimulation, as determined by the enhanced expression levels of TNF-α, IL-6 and IFNβ1, key markers of STING-mediated downstream effector activation.