The resulting association of mutant clone size and risk of death in this population could not be explained by CHIP carriers holding a worse HF baseline risk, as measured by alterations in left ventricular ejection fraction, known HF risk scores and serum levels of N-terminal pro-B type natriuretic peptide; thus, HF behaves definitely as a “bona fide” cardiovascular complication of CHIP. This evidence concerns the gene STUB1 and hydrops fetalis.