Since there is no evidence that NF-κB has the ability to initiate chromatin remodeling (reviewed in [40]) it is likely that the the above analogies reflect synergism between NF-κB and some unknown constitutive or induced pioneer transcription TF(s); possibly from the Stat or Irf families, which have overlapping targets and similar roles in development and cancer (e.g. [144, 145]). The gene discussed is SOAT1; the disease is cancer.