Indeed, the CaM antagonists trifluoperazine (TFP) and ophiobolin A induced a dose-dependent inhibition of tumor cell migration, an additional inhibition of tumor cell proliferation at higher concentrations and sensitized the cells to TG)-induced ER stress—the same effects that were reported for Sec62-depleted tumor cells.89–91 Hence, a treatment with CaM antagonists represents a potential mechanism how to achieve a functional SEC62 knockdown in a living organism and thereby inhibiting the migratory and proliferative potential of tumor cells. This evidence concerns the gene SEC62 and neoplasm.