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A tight control is needed to adjust each enzymatic step to the cellular requirements because the whole pathway consumes energy and produces toxic/reactive compounds, notably sulfite and sulfide

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showed that loss of ABHD5 promotes YAP-induced c-MET overexpression which in turn increases and sustains the stemness of CRC cells and promotes the development and progression of CRCs ( Bardelli and others showed that the multi-kinase inhibitor, crizotinib could overcome primary and secondary resistance to anti-EGFR caused by MET amplification in patient-derived CRC xenografts ( de novo and acquired cetuximab resistant CRC cell lines, SC and CC-CR, respectively, that are WT for KRAS, BRAF, PIK3CA, and EGFR, and not amplified MET, but with increased MET/RON tyrosine phosphorylation ( in vitro against CRC cells HT-29, HCT-116, SW-480, and DLD-1 and in vivo in HT-29 xenograft model, indicating a promising combination approach for the treatment of advanced CRC ( in vitro and in vivo in KRAS-mutated CRC cells (Van Schaeybroeck et al., 2014)