“…A large number of somatic and germinal mutations (EGFR (20%), TP53 (54.6-64.6%), KRAS (43.7%), BRAF (3.2%), ERBB2 (1.3%), MET (9.4%), STK11 (16.2%), and PIK3CA (9−12.4%)), gene amplifications (EGFR, ERBB2, MET (17.68%), PIK3CA, and NKX2), deletions (DOK2), rearrangements (ALK (13.3%), ROS1 (3.9%), and RET (5.2%)), and fusions (ALK/EML4) [31], which increase the risk of developing lung cancer in certain populations, have been identified but have not led to the development of effective treatments since global mortality rates have not significantly decreased [9]. TP53 (78%), TTN (68%), CSMD3 (39%), MUT16 (36%), and RYR2 (36%) have the highest mutational frequency, and BRINP3, COL11A1, GRIN2B, MUC5B, NLRP3, and TENM3 have shown significantly higher mutational frequency in stage III of lung squamous cell carcinoma [32], while TP53, EGFR, KRAS, ALK, BRAF, MET, RET, and ROS1 are the most frequent mutation genes in lung adenocarcinoma [33]. KRAS mutations appear in less than 40% of NSCLC patients, with a higher prevalence in LUAD (32%) than in LUSC (4%), in Western (26%) than in Asian (11%) patients, in smokers (30%) than in non-smokers (10%), and almost never in SCLC [34].…”