Moreover, Smad3 activation in CAFs contributes to the NSCLC progression in the NSCLC cohort studies.[48] Surprisingly, unbiased gene network analysis uncovered a unique Smad3‐centric gene network as the key regulatory mechanism of MMT in NSCLC, which is different from the case of kidney disease where an Src‐centric network was identified.[28] Specifically, macrophage‐specific silencing of Smad3 successfully prevented the transferred BMDM undergoing MMT in vivo, resulting in a dramatic reduction of CAF population, neo‐angiogenesis, and tumor growth. The gene discussed is SRC; the disease is kidney disorder.