The requirement for Hsp90 in cancer cells, virally infected cells or cells that accumulate misfolded proteins seems to be so profound that it translates into selectivity in clinical settings for second generation Hsp90 inhibitors; alternatively it has been suggested that the hsp90 multi-protein complex differs between tumor cells and normal cells and that this would result in increased drug access to the Hsp90 ATP binding sites. This evidence concerns the gene HSP90AB1 and cancer.