One plausible explanation is that blocking SRC inhibits both CRIPTO1-mediated AKT and p44/42 MAPK signaling and EMT, both of which are required for the reversal of CRIPTO1-induced erlotinib resistance.
Although blocking ZEB1 compromises EMT, SRC-mediated AKT and p44/42 MAPK signaling may be sufficient to sustain erlotinib resistance in CRIPTO1-positive, EGFR-mutated NSCLC cells.