At the endpoint of our present study, the DOXO-induced LV wall thinning, systolic dysfunction, and cardiac fibrosis were associated with the overexpression of selected elements of the fibrotic TGF-β/SMAD signaling pathway (i.e., Ctgf, TGFβRII, Smad2, Smad3, and Col1a1) and molecular markers of apoptosis (i.e., Bax, and Bax/Bcl2 ratio), cardiac remodeling (i.e., Mmp2 and Mmp9), heart failure, (i.e., Nppa and Nppb), inflammation (i.e., Il1, Il6, and Tnf) and nitro-oxidative stress (i.e., Nos2). The gene discussed is COL1A1; the disease is heart failure.