Further functional assays showed that depleting endogenous PS (via PSS1 knockdown) or mislocalizing PS from the PM (via treatment of fendiline to inhibit acid sphingomyelinase) effectively compromised the KRAS-regulated phosphorylation of RAF/MEK/ERK in the MAPK cascade and the proliferation of the mutant KRAS-dependent human tumor lines, without affecting the KRAS-independent human tumor lines. Here, KRAS is linked to neoplasm.