This includes characteristics such as the genetic-, functional- and histological features of the patient’s tumor, along with sequential mutagenesis (i.e., loss of adenomatous polyposis coli, APC), followed by activating Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations and loss of TP53, the presence of stromal- and immune cells, as well as the presence and composition of tumor stroma. Here, KRAS is linked to neoplasm.