Furthermore, the genomic landscape of the high-risk group revealed frequent copy number gains in oncogenes such as EGFR, SLC2A1, and HIF-1 A alongside losses in key tumor suppressors like PTEN, TP53, BRCA1, ERCC1, and CDKN2A. These alterations are consistent with activation of proliferative and survival pathways, including PI3K/AKT signaling and NER, which are known contributors to treatment resistance and poor prognosis in resected NSCLC (Rose-James and Tt 2012). The gene discussed is AKT1; the disease is non-small cell lung carcinoma.