Since the obtained data clearly pointed to increased regulation of S1P production and a metabolic shift favouring the production of specific long-chain and very long-chain ceramide species as molecular features of acquired resistance to vemurafenib, we hypothesized that either inhibiting sphingosine kinases 1 and 2 or retuning the ceramide balance by exogenous short-chain C6 ceramide could restore vemurafenib sensitivity in resistant BRAF mutant colon cancer cells. The gene discussed is SPHK1; the disease is colonic neoplasm.