In GBM, NR4A2 activates SQLE to dysregulate cholesterol homeostasis in non-tumor stromal microglia, and the pharmacological blockade of NR4A2 or SQLE can augment immune checkpoint blockade therapeutic efficacy; particularly, terbinafine and anti-PD1 induced tumor regression and prolonged survival for GL261-luc-bearing mice compared with each monotherapy or treatment control [51]. The gene discussed is NR4A2; the disease is neoplasm.