Together, these suggest the contribution of multiple cell-types in myofibroblast transformation in subretinal fibrosis, and repression of <i>miR-24</i>-regulated TGF-β/SMAD3 and PAK4/LIMK2/MRTF pathways in multiple cell types holds therapeutic potential for treating subretinal fibrosis in AMD and other fibrotic disorders. Here, SMAD3 is linked to age-related macular degeneration.