PRKCI and lung adenoma: While genetic ablation of Prkci (encoding PKCi protein) block BASCs expansion and subsequent lung adenoma formation in response to oncogenic Kras [60], recent work demonstrated that PKCi expression favors BASCs-derived LUAD and PKCi-dependent tumors through the activation of PKCi/ELF3-NOTCH3 signaling, while Prkci deletion leads to Axin2+ AT2-derived LUAD that are PKCi-independent and exhibit dependency upon Wnt/β-catenin signaling for their growth and stem-like activity [51].