FLI1 and Familial prostate cancer: Aberrations, including recurrent mutations in SPOP1, FOXA1, IDH1, fusions in TMPRSS/ERG, ETV1/4, FLI1 and copy number alterations, such as MYC amplification or NKX3-1, RB1 and PTEN deletions or transcriptomic changes in AMACR, PCA3, GDF15 and MSMB, have all been investigated in the context of prostate cancer.5–7 Over the past 5 years, there has been an increased effort to use this to develop our understanding of the genetic basis of prostate cancer conspicuity on mpMRI.