To this aim, the sensitivity to membrane-permeant peptides inhibiting either JNK activation (Tat-JIP) or destabilizing the VANGL2–p62/SQSTM1 interaction (FITC-Tat-p62DN) was evaluated in a proliferation assay on four breast cancer PDX-derived cell lines expressing high (PDX 13 and 26) or low (PDX 2 and 27) levels of VANGL2 that correlated with phospho-JNK contents (Supplementary Fig. 7). Here, SMAD4 is linked to breast carcinoma.