Due to strongly impaired HR activity in the NES-mutated cells, the persistent DSBs lead to formation of chromosome aberrations and most importantly, they trigger senescence and SASP, as shown by induction of IL6 and IL8. This is highly important since, as a putative tumor-suppressing mechanism, SASP can reinforce the growth arrest by increasing ROS production and enhancing DDR [40]. Here, IL6 is linked to neoplasm.