BCL2 and neoplasm: In addition, treatment with H‐EVs and overexpressed EGFR induced up‐regulation of the proliferation marker Ki‐67, down‐regulation of the tumor‐suppressor gene PTEN, and activation of anti‐apoptotic responses (increased Bcl‐2 and inhibited Bax expression) in 6–10B and S26 cells, which was inverted by EGFR‐KO H‐EVs treatment or EGFR knockdown (Figure 5g).