CDKN2A and Miyoshi myopathy: Molecular analyses of cell lines from Htz Bap1 mice showed Bap1 LOH, but no alteration of Ink4a, Ink4b and Arf, in contrast to WT mice that retain WT Bap1, but were deleted in Ink4a, Ink4b and Arf, suggesting two alternative mechanisms of MM development despite the fact that CDKN2A and BAP1 mutations are not exclusive in HMM [76].