Figure 5. Schema indicating how HSP90, and hence its inhibition by nelfinavir (NFV) sit at several crossroads previously documented as crucial for glioblastoma growth.

Note that CUSP9 is expected to inhibit the compensatory survival-enhancing response to temozolomide by two paths. A) as indicated in this Figure via nelfinavir dampening of AKT function, and B] by the NFkB degradative actions of disulfiram. Maintainance of a good NFkB pool is one of the crucial elements in glioblastoma hardiness [314].