For example, advanced glycation end products (AGEs) could activate Smad2/3 early phosphorylation through ERK/p38.64 And STMN-2, markedly up-regulated in HCCs, could activate Smad2 independent of TGF-β1 stimulation.65 Therefore, whether TGF-β1-independent Smad regulator is involved in Smad-downregulated SYK in NSCLC needs further exploration. Here, STMN2 is linked to non-small cell lung carcinoma.