Here, to determine if themacropinocytosis-mediated cellular uptake of CaP-rHDL is Ras-dependent, weemployed the cell lines including human glioblastoma cell lines U87 and U251,human pancreatic adenocarcinoma cell line MIA PaCa-2 (KRas G12C mutation)and colorectal cancer cell line SW-480 (KRas G12V mutation), all showedhigher Ras activity than astrocytes, a pancreastic cell line BxPC-3 and a coloncell line Caco-2, which express wild-type KRas32, 33, 34, 35, for the analysis. The gene discussed is KRAS; the disease is pancreatic adenocarcinoma.