We hypothesize that activating mutation of KRAS inducing expression of molecules responsible for interaction with platelets, such as tissue factor [26], cyclooxygenase and metalloproteinase-9 [27], or cathepsin B [28] might contribute to increased protection of these carcinoma cells against shear stress as well as to enhanced adhesion properties which in turn leads to onset of pulmonary metastasis of mutated KRAS carcinoma cells and higher metastatic activity in general [29]. This evidence concerns the gene KRAS and carcinoma.