Considering tumor-adaptative response related to sustained AMPK signaling (104), drug-efflux (89) or iNOS/NO axis (123), the combination of 5-ALA-PDT with positive modulators of the autophagic machinery (e.g. rapamycin), regulators of iNOS and drug-extrusion, NO scavengers, or NFκB inhibitors should be considered to increase clinical outcomes (93, 100, 103, 114–120, 147). The gene discussed is NFKB1; the disease is neoplasm.