However, considering that excessive SLX4 itself can trigger the collapse of stalled replication forks and subsequent DNA breakage, potentially yielding opposing effects by facilitating break-induced replication (BIR) (Dilley et al, 2016; Roumelioti et al, 2016; Zhang et al, 2019), selecting appropriate ATR concentrations for treatment in different ALT cancer cell lines might be a critical consideration. Here, SLX4 is linked to cancer.