Data from Jongsma et al. [59] suggest a prominent role of Cdkn2a and Trp53, compared to Nƒ2, as mice harbouring Hom Nƒ2 and either Htz Cdkn2a or Htz Trp53 have longer survival than mice with Hom Cdkn2a or Trp53 and Htz Nƒ2. However, Htz Trp53 in association with Htz or Hom Tcs1 did not induce MM, contrary to its association with Nƒ2, but consistent with a bona fine role of Nƒ2 in MM [58,59]. This evidence concerns the gene TP53 and Miyoshi myopathy.