Although only ELF3 was demonstrated as a crucial regulator of E-cadherin in Shimamura et al., [1], interactions FLI1 and TP63 with E-cadherin are also verified as follows: Cav1-Snail-E-cadherin pathway plays a central role in the expression of the oncogenic transformation functions of fusion gene EWS/FLI1 [57]; reactivation of △Np63a is linked to the maintenance of epithelial markers and suggests that E-cadherin has a dual role in lung squamous cell carcinoma [58]. Here, CAV1 is linked to squamous cell lung carcinoma.