CASC3 and Miyoshi myopathy: Different molecular mechanisms have been proposed to explain BTZ resistance in MCL and MM, for instance mutations/alterations in the β5 subunit, crosstalk with other proteolytic pathways, engagement of endoplasmic reticulum, oxidative stress response, epigenetic, and microenvironmental factors, among others, leading the scientific community to consider BTZ acquired resistance as a multifactorial event [6–9].