While correlated to low expression of HRR genes, bi allelic CDK12 inactivation was more recently shown to be associated with a distinct subgroup of prostate cancers characterized by focal tandem duplications and gene fusion-induced neoantigens all over the genome, as well as CD4 + FOXP3—tumor-invasive lymphocytes (i.e., likely to be permissive) [28, 33]. This evidence concerns the gene CDK12 and prostate carcinoma.