This case files a bloodstream infection caused by a VRSA stress in an individual with a serious skin condition that probably predisposed the individual to bacterial colonization. The individual was treated repeatedly with beta-lactams and glycopeptides, and our analyses claim that the MRSA isolate had acquired the vanA plasmid during therapy also. The genetic characterization and genomic analyses also suggest that the vanA gene cluster within BR-VRSA may have originated from an enterococcal donor. The DNA sequence of the vanA gene cluster of BR-VRSA is similar to the sequence within the genome of VREF that was recovered from a swab of the patient’s rectum, suggesting that VREF might have been the donor.Quality 4 hematologic toxicity was experienced by 96 percent of patients during induction, in addition to which there have been 51 patients with quality 3 and three patients with grade 4 febrile neutropenia. There were eight deaths during induction. During consolidation, 98 percent of patients had grade 4 hematologic toxicity, plus 15 patients had grade 3 and one patient quality 4 febrile neutropenia, and 12 patients had quality 3 and two patients quality 4 clinically documented infections. There is one treatment-related loss of life. The researchers see in the Journal of Clinical Oncology: ‘Strategies such as altering the route of administration of bortezomib from IV to subcutaneous, changing the plan from twice to once per week, or using other proteasome inhibitors with much less neurotoxicity, such as carfilzomib, may reduce neurotoxicity without sacrificing clinical efficacy; these approaches warrant investigation in long term clinical studies.’ Median follow-up for 34 surviving sufferers was 22 weeks.