Interestingly, these authors microdissected the IDC and IC components of six sporadic BRCA2-mutant prostate cancers bearing IDC: both IDC and IC components arose from the same founding clone, with no evidence of multiple tumors; the parental population was found both in the IDC and IC regions; MYC amplifications observed in 75% of these four cases and always occurred before divergence of the IDC and IC components; in contrast, the MED12L gain was clonal in 50% of cases and subclonal in the other 50% of cases [30]. This evidence concerns the gene MED12L and prostate carcinoma.