For the other scientists out there, the present
study appears very consistent with the impaired sphingosine-1-phosphate (S1P) signaling hypothesis (see my signature), and I believe the findings are what would be expected if either S1P levels are too low or if there are autoantibodies against a S1P receptor.
S1P signaling is a critical regulator of intracellular calcium concentration/flux and is mediated by S1P both through its receptors (e.g., S1PR1 aka S1P1) on the cell surface and also within the cell itself independently of any receptor. (There are several dozen potential references. See this
PubMed search string.)
So, IMO, the TRPM3 receptors are not going to be the primary problem here, but rather impaired S1P signaling, and the modest reductions in function that any single nucleotide polymorphisms (SNPs) in the TRPM3 gene may be making are likely just exacerbating the problem.