That our drug combination: (a) reduced HSP70: AIF co-localization in the cytosol; (b) increased eIF3A: AIF association in the nucleus; and (c) reduced total HSP70 expression, strongly argues that the upstream mTOR inhibition/ER stress-autophagy-BAX/BAK/BID-dependent AIF release from the mitochondria and the facilitation of its translocation to the nucleus is very likely the key mechanism by which our (ruxolitinib + afatinib) drug combination was killing tumor cells. The gene discussed is AIFM1; the disease is neoplasm.