In an effort to identify clinically actionable pathways downstream of E-cadherin loss, Derksen and colleagues used CRISPR/Cas9 knockouts to show increased growth factor receptor (GFR)-dependent activation of PI3K/Akt signalling; treatment with Akt inhibitors resulted in robust inhibition of tumour growth in their murine ILC models [125]. Here, CDH1 is linked to neoplasm.