Nonetheless, though androgens may not directly transform normal prostate cells, accumulating data hint that AR signaling may play a role in the progression of transformed prostate cells to invasive carcinoma cells, as indicated by order and timing of molecular events in prostatic carcinogenesis, particularly the propensity for gene fusions leading to AR-regulated ETS family oncogene expression to appear later than MYC activation, telomere shortening, and epigenetic gene silencing (55). Here, AR is linked to invasive carcinoma.