However, activation of different kinases such as ERK, p38, JNK, MAPK, CDKs, and ROCK, has been shown to induce the phosphorylation of SMAD2 and SMAD3 in their linker regions, which results in altered transcriptional activity of the SMAD2/3 complex and the functional switch from apoptosis to EMT and tumor progression [143,144]. The gene discussed is SMAD2; the disease is neoplasm.