Due to the profound heterogeneity exhibited amongst patients with lung adenocarcinoma (LUAD), considerable variances in clinical efficacy emerge.1 For the aims of precision medicine, a clinical instrument to delineate distinct disease phenotypes and anticipate susceptibility to intervention is imperative. Cellular cytotoxicity mediated through T lymphocytes constitutes a pivotal mechanism of anti-tumoral immunity and the foundation for cancer immunotherapy.2 Numerous genes regulating the sensitivity of tumor cells to killing mediated by T lymphocytes (GSTKKs) are conducive to satisfying the aforesaid medical necessity.