In summary, our work reveals that Cav3 associates with lysosomal membranes and that loss of Cav3 induced by myocellular expression of the LGMD‐1C Cav3P104L mutation or targeted Cav3 gene deletion in vivo or in vitro is associated with a reduction in mTORC1 signalling capacity, which we suggest is likely linked to changes in lysosomal cholesterol content/trafficking. Here, CAV3 is linked to rippling muscle disease 2.