For example, treatment with drugs that inhibit enzymes that act early in the de novo Cer-SM biosynthetic pathway (fumonisin B1, myriocin, GT11 or K1), acid sphingomyelinase (ASM) inhibitors (fendiline, desipramine, imipramine, and amitriptyline), or sphingomyelin synthase 1 (SMS1) activators (2OHOA) have been shown to promote K-Ras mislocalization by altering the SM and PS content and organization in the cell, affecting pancreatic cancer [205]. This evidence concerns the gene SMPD1 and familial pancreatic carcinoma.