In fibroblasts, while it was shown to barely activate cyclic adenosine monophosphate (cAMP), which is postulated to be associated with tumor growth [9], B7-33 activated the pERK pathway with a potency similar to H2 relaxin [9], and pERK activation is known to link to the anti-fibrotic and vasodilatory effects of H2 relaxin [4,14]. This evidence concerns the gene EIF2AK3 and neoplasm.