Cancer cells themselves can activate STING via various mechanisms including the accumulation of DNA induced by chemoradiation, senescence or CIN thereby leading to the production of IFNβ.[11, 13] Deficiency in STING, demonstrated through knockout studies of Tmem173 or Irf3, correlated with lower T cell infiltration and resistance to ICIs in murine models.[25]. This evidence concerns the gene STING1 and cervical squamous intraepithelial neoplasia.