Mutant KRAS tumors are highly associated with other classic driver mutations such as TP53, SMAD4, and CDKN2A, while KRAS wild-type tumors are characterized by downstream RAS/RAF/MAPK/PI3K-activating mutations, increased mutation rates of ERBB2 (HER2) and ATM, and increased tumor mutational burden (TMB) [7,8]. The gene discussed is SMAD4; the disease is neoplasm.