A priori, linker phosphorylation of SMAD2 seems to be responsible for maintaining cellular differentiation and is associated with a favourable prognosis, while the short splice variant is induced upon loss of linker phosphorylation, thereby enhancing pluripotency protein levels and directing NSCLC towards de-differentiation (Fig. 5f, g). Here, SMAD2 is linked to non-small cell lung carcinoma.