The study identified that both classes more commonly co-mutated with TP53, KRAS, STK11, and KEAP1 mutations as compared to these co-mutations in a SMARCA4 wild-type tumor, and to a lesser extent, it is not uncommon to have co-alterations with other oncogene drivers, i.e., EFGR mutation. This evidence concerns the gene TP53 and neoplasm.