Additionally, we found potential SL relationships between TP53 (cluster 2) and TP53BP1 (cluster 3), and CHEK2 (cluster 3) with PARP1 (cluster 1) that has not been reported previously but show clinical benefits upon co-inactivation in lung adenocarcinoma (LUAD) and prostate adenocarcinoma (PRAD), respectively. This evidence concerns the gene TP53 and prostate adenocarcinoma.