Johnson et al. [70] demonstrated how cyclin-dependent kinase 1 (CDK1) is deeply implicated in HR, since CDK1-mediated BRCA1 phosphorylation constitutes an essential step for HR machinery effector scaffolding upon DNA DSBs: by combining CDK1 and PARP inhibition, they obtained reduced cell colony formation, disrupted human tumor xenograft growth and tumor regression leading to improved survival in a mouse model of BRCA WT lung adenocarcinoma. This evidence concerns the gene PARP1 and lung adenocarcinoma.