Independently of the mechanism, preventing Ca2+ influx may be beneficial and holds potential for future therapeutic strategies to tackle muscular dystrophy either by targeting STIM1/Orai1 or TRPC channels, since both channel complexes have been shown to be implicated and/or up-regulated in Duchenne muscular dystrophy models [75,106]. Here, STIM1 is linked to Duchenne muscular dystrophy.