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. Here, AMACR is linked to Familial prostate cancer.