SMARCAL1, an ATP-dependent chromatin-remodeling protein, belongs to the SNF2-family DNA translocase. It has crucial functions in DNA repair, genome stability maintenance, and transcriptional co-regulation. It participates in DNA damage response pathways, such as reannealing stalled replication forks in response to DNA damage [2].

SMARCAL1 loss in a mouse melanoma model hinders tumor cells' ability to induce PD-L1 in response to genomic instability, enhances anti-tumor immune responses, and sensitizes tumors to immune checkpoint blockade, suggesting it promotes tumor immune evasion through suppressing innate immune signaling and inducing PD-L1-mediated immune checkpoint responses [1]. In telomerase-negative glioblastoma cells, SMARCAL1 deficiency promotes alternative lengthening of telomeres and tumorigenesis [3].

In conclusion, SMARCAL1 is essential for maintaining genome stability, regulating immune responses related to tumors, and controlling telomere-associated processes. The study of SMARCAL1 knockout models has provided valuable insights into its role in tumor-related immune evasion and tumorigenesis, potentially offering new targets for cancer immunotherapy and treatment strategies.