Once the data had been segregated, gene-sets with very powerful clinical outcome parameters were discovered. Over the next 24 hours, the E2F1- and E2F2-transduced lines underwent growth arrest, suggesting that these lines are still susceptible to contact inhibition. However, the E2F3-transduced line continued to grow at the same rate 24 hours after reaching confluency, suggesting that forced expression of E2F3 can overcome contact inhibition. Conversely, 3T3 cells with forced expression of E2F1, E2F2 and E2F3 continued to grow following serum deprivation. E2F2- and E2F3-transduced cultures continued to double after 16 hours of serum withdrawal, and maintained at least two-fold greater cell numbers than control cultures throughout the 48 hour culture period. E2F1-transduced cultures showed a more modest rate of growth, however, these cultures were also able to maintain significantly increased cell numbers throughout serum deprivation as compared to empty vector-transduced cultures. Unlike the lines with forced expression of E2F1, 2 or 3, cell lines transduced with E2F4, E2F5 and E2F6 did not continue to grow following serum withdrawal, and maintained cell numbers equal to or less than the control-transduced cultures throughout the entire response. These data show that uncoupling of E2F1, E2F2 and E2F3 expression from their normal growth factor-mediated regulation is sufficient to drive a significant degree of growth factor-independent cell cycle progression, but that E2F4, 5 and 6 cannot mediate this effect under the same conditions. It was also obersved that there was significantly expression of CaP biomarkers that those of white men, one of which was the AR. By identifying such protective pathways of AR function, along with identifying powerful prognostic tools to predict disease, now we can assess pathways to also offer novel therapeutic targets.