Organization of the Ca2+ transients into clusters was due to voltage-dependent Ca2+ entry that appeared to be due to activation of both high-voltage activated Ca2+ channels (L-type encoded by Cacna1c and Cacna1d in ICC-SM) and low-voltage activated Ca2+ channels (T-type encoded by Cacna1h and possibly Cacna1g in ICC-SM). This evidence concerns the gene CACNA1D and intrahepatic cholangiocarcinoma.