Indeed, both PKCα and PKCε have long been implicated in breast cancer progression and the EMT of breast cancer cell lines (40, 41, 42, 43, 44), and an excellent body of work from the Rotenberg laboratory has firmly established α6-tubulin and CEP4 as direct targets of PKCα underlying robust changes in morphology and motility of MCF-10A cells upon stable overexpression of this kinase within them (28, 45, 46, 47, 48). The gene discussed is PRKCA; the disease is breast carcinoma.