One notable example is the co-occurrence of oncogenic driver alterations, such as KRAS and EGFR mutations, along with the inactivation of well-known tumor suppressor genes like tumor protein p53 (TP53), LKB1 (STK11), and KEAP1. These co-occurring patterns have significant biological implications and can influence tumor evolution and progression (18). Here, KRAS is linked to neoplasm.