We orthogonally confirmed recruitment of the key adaptor, GRB2, to endogenous EML4-ALK cytoplasmic protein granules detected by IF in patient-derived cancer cells (H3122) (Figure 2D), as well as through dual expression of EML4-ALK and GRB2 in Beas2B cells (Figure S2B). This evidence concerns the gene EML4 and cancer.