Using ncDHPR mice, in which skeletal muscle (CaV1.1) Ca2+ channels are rendered nonpermeable to Ca2+ by point mutation (Dayal et al, 2017, 2021), we show that excessive Ca2+ influx through CaV1.1 is not responsible for myopathy arising from KATP LoF which argues against the use of Ca2+ channel blockers (CCBs) for treatment of AIMS symptoms. The gene discussed is CACNA1S; the disease is myopathy.