In addition, from the experience in kidney diseases, macrophages can regulate myofibroblast formation via both direct and indirect pathways.[49, 50] Additional research has indicated that tumor‐associated macrophages are capable of inciting myofibroblast activation in the tumor microenvironment through their secretome.[51, 52, 53] The pronounced reduction of total α‐SMA seen in LLC‐bearing macrophage‐specific Smad3 conditional knock‐out mice intimates a potential function of Smad3 in the macrophage‐driven activation of CAF in NSCLC. The gene discussed is ACTA1; the disease is kidney disorder.