Furthermore, overexpression of SKIL increased expression of SLUG and vimentin, decreased E-cadherin expression, as well as increased levels of cancer stem cell markers (CD44, SOX2, OCT3/4) and autophagy markers (LC3, p62, Beclin-1), while further TAZ silencing reversed the effect of SKIL on those markers compared to SKIL overexpression group (Fig. 5f–i). This evidence concerns the gene SKIL and cancer.