Lu et al. proposed a mechanism of EMT-dependent inhibition of apoptosis where loss of E-cadherin (which binds selectively to DR4 and DR5 but not to Fas owing to the DISC formation and caspase-8 activation) drives cancer-cell resistance to TRAIL treatment.79 Another study reported that EMT reversal by ML327, an isoxazole-based small-molecule probe that represses E-cadherin levels and partially reverses the EMT phenotype, is accompanied by an enhanced response to TRAIL in carcinoma cells and this was in an E-cadherin-independent manner.122. The gene discussed is FAS; the disease is cancer.