TP53 and Miyoshi myopathy: For instance, miR-106b-25 cluster, miR-181a, miR-181b and miR-32 were found to be upregulated in MM, favoring oncogenesis due to their capacity to downregulate the p53 tumor suppressor by controlling the expression of PCAF, a histone acetyltransferase involved in transcription control of TP53 [197].