However, other results indicate that in the post-ischemic heart of mice, the increase in Cers appears to be mediated more by acid sphingomyelinase than by de novo sphingolipid synthesis, but the inhibition of acid sphingomyelinase and the consequent reduced Cer levels do not improve heart function or survival after AMI, opening doubts about the final benefits of targeting acid sphingomyelinase as a treatment for the ischemic heart disease [105]. Here, SMPD1 is linked to benign neoplasm.