SNAI1 and neoplasm: Thus, activation of the TGF-β signaling pathway [65,67,68,81]—modulated by miR-29c and miR-192 [81]—leads to overexpression of primary drivers of a mesenchymal phenotype (ZEB1/2, TWIST, GLI1/2, and SNAI1/2) [10,24,37,57,65,68,69,80,82], while upregulation of the TP63ΔN transcriptional network in the presence of TP53 mutations [10,74], and hypermethylation of the MET receptor [37], regulate tumor cell plasticity and proliferation allowing for the development and establishment of a squamous PDAC transcriptional profile.