Furthermore, we investigated the somatic mutations of tumor driver genes in both clusters, including TP53, KRAS, STK11, EGFR, and KEAP1. The results showed that cluster 2 possessed a higher overall mutation rate and higher mutations in KRAS, STK11, and KEAP1 genes compared to cluster 143 (Fig. 2B). This evidence concerns the gene EGFR and neoplasm.