SPHK1 and colorectal cancer: Down-regulation of SphK1 activity by pharmacological inhibitor N,N-dimethylsphingosine (DMS) (Figure 3) or siRNA restored sensitivity to cetuximab in colorectal cancer cells with intrinsic or acquired resistance to cetuximab, whereas over-expression of SphK1 precluded cetuximab-induced apoptosis [61].