Treatment with LNA‐miR‐29 visibly increased fibrous cap thickness in both roots and BC (Fig 2A, quantified in Fig 2B) and levels of immunoreactive smooth muscle actin (SMA; Fig 2C and D) but not the abundance of a macrophage marker (CD68), proliferating cells (Ki‐67), or an apoptotic marker (TUNEL; Figs EV3 and EV4), indicating a relatively quiescent population of VSMC in LNA‐miR‐29‐treated group. The gene discussed is SMN1; the disease is breast cancer.