Our previous data demonstrate that in SSc-ILD myofibroblasts, IQGAP1 shuttles monomeric SMA, facilitating its assembly through a mechanism distinct from β- and γ-actin polymerization [8], which suggests that shuttling monomeric SMA results in the increased rate of SMA polymerization and organization in lung fibroblasts. The gene discussed is IQGAP1; the disease is systemic sclerosis.