Most notably, compared to the expression of flanking exons in UMSCC-74B cells, CELF1 depletion caused a 5-fold increase in the exclusion of exon 49 in COL16A1 (collagen type XVI), which encodes an extracellular matrix protein involved in oral cancer cell proliferation and glioma cell invasion (Figure 2C) [45, 46]. The gene discussed is COL16A1; the disease is central nervous system cancer.