Considering the roles of CD24, CD44, and MCT1 in regulating a CSC-like phenotype, we suggest that the acquisition of metabostemness induces establishment of pancreatic cancer cells that exhibit different degrees of anchorage-independent growth and invasive properties based on the relative levels of CD24, CD44, and SLC16A1 (Supplementary Fig. 6d). This evidence concerns the gene SLC16A1 and familial pancreatic carcinoma.