The differential responses of PKC, mTORC1, and MAPK of the two types of cancer cells to loss-of-EGFR indicate that the KID functions of regulating these pathways are cell type dependent, and the commonality of mTORC2/Akt in mediating loss-of-EGFR-induced mitophagy among the different cell types argues that this EGFR’s kinase-independent anti-mitophagy pathway is a more fundamental mechanism. The gene discussed is PRRT2; the disease is cancer.