Whether the pathologists omitted the tumor cells in the face of a large number of PMP surgical specimens, whether the cell-free DNA of KRAS mutation played a role as suggested by García-Olmo et al. [197], or whether it was the colonization of Pseudomonas [86] or other reasons, the mechanism of this kind of tumor cell-independent mucin production merits further discussion. The gene discussed is KRAS; the disease is neoplasm.