text: Yo, check it out, I got a story to tell,
  'Bout miR-138 and its impact on cardiac cells.
  In zebrafish, it's known to modulate morphogenesis,
  But what 'bout humans? Let's dive into the genesis.
  
  We conducted a study, case-control design,
  With 857 CHD cases, 938 controls combined.
  Genotyping miR-138, looking for SNPs,
  To see if they contribute to congenital heart disease.
  
  Two variants we found, let me break it down,
  First is rs139365823, rare but renowned.
  It's located in the pre-miR-138 sequence, you see,
  And it's linked to CHD, statistically.
  
  The second SNP, rs76987351,
  In the pri-miR-138 sequence, let's have some fun.
  No association with CHD, we found,
  But hold up, there's more, let me go another round.
  
  Real-time PCR data, we got the facts,
  rs139365823, minor allele A impacts.
  It increases mature miR-138 expression,
  While rs76987351 goes in the opposite direction.
  
  Now, let's talk about the mechanism, you know,
  Tetralogy of Fallot, a subtype that can throw,
  Severe outflow tract development off track,
  And miR-138's involved, that's a solid fact.
  
  Dvl2, a player in outflow tract formation,
  MiR-138 targets it, causing some alteration.
  And guess what? The minor allele A,
  Enhances miR-138's inhibitory sway.
  
  So, to sum it up, let's make it clear,
  The variant rs139365823, you should fear.
  It alters miR-138 expression and its effect,
  Increasing the risk of CHD, that's what we detect.
  
  This study sheds light on the population we examined,
  The first to show how this variant's implicated.
  In congenital heart disease, it plays a role,
  MiR-138 and its SNPs, now you know the whole.