CAV1 and multiminicore myopathy: For example, potential changes to the extent and configuration of the Cav-1 K48 and K63 ubiquitination chains by the mutations could disrupt the regulatory balance between protein degradation, signal transduction, and cellular energetics, and lead to a dysregulated Cav-1 pool [35,89] that impairs its role in maintaining endothelial cell integrity and vascular function or lead to altered inflammatory or apoptotic responses [21] that promote the vascular occlusion observed in MMD patients.