Since the most common EGFR-independent resistance mechanisms involve reactivation of RTK/RAS/effector pathways (Mancini et al., 2018; Romaniello et al., 2018; La Monica et al., 2017; Eberlein et al., 2015), we wanted to assess whether inhibition of different proteins within the EGFR/RAS signaling pathway could synergize to inhibit 3D survival of EGFR (T790M) mutated cancer cells. This evidence concerns the gene EGFR and cancer.