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Sorafenib\/regorafenib and the multi\u2010kinase inhibitor pazopanib (Votrient) interacted with sildenafil (Viagra) to further rapidly reduce GRP78 levels in eukaryotes and as single agents to reduce Dna K levels in prokaryotes. Similar data were obtained in tumor cells in vitro and in drug\u2010treated mice for: HSP70, mitochondrial HSP70, HSP60, HSP56, HSP40, HSP10, and cyclophilin A. Prolonged \u2018rafenib\/sildenafil treatment killed tumor cells and also rapidly decreased the expression of: the drug efflux pumps ABCB1 and ABCG2; and NPC1 and NTCP, receptors for Ebola\/Hepatitis A and B viruses, respectively. Pre\u2010treatment with the \u2018Rafenib\/sildenafil combination reduced expression of the Coxsackie and Adenovirus receptor in parallel with it also reducing the ability of a serotype 5 Adenovirus or Coxsackie virus B4 to infect and to reproduce. Sorafenib\/pazopanib and sildenafil was much more potent than sorafenib\/pazopanib as single agents at preventing Adenovirus, Mumps, Chikungunya, Dengue, Rabies, West Nile, Yellow Fever, and Enterovirus 71 infection and reproduction. \u2018Rafenib drugs\/pazopanib as single agents killed laboratory generated antibiotic resistant <jats:italic>E. coli<\/jats:italic> which was associated with reduced Dna K and Rec A expression. Marginally toxic doses of \u2018Rafenib drugs\/pazopanib restored antibiotic sensitivity in <jats:italic>pan\u2010antibiotic resistant<\/jats:italic> bacteria including multiple strains of <jats:italic>bla<\/jats:italic><jats:sub>kpc<\/jats:sub> <jats:italic>Klebsiella pneumoniae<\/jats:italic>. Thus, Dna K is an antibiotic target for sorafenib, and inhibition of GRP78\/Dna K has therapeutic utility for cancer and for bacterial and viral infections. J. Cell. 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