Phipps et al. in 1994 performed Fluorescence in Situ Hybridization (FISH) on GM10922, GMTPL, a new case [46, XX, del(3)(p25p26)] with an atrial septal defect (sample CUMG3.4) and two more carriers of the 3p- syndrome without CHDs.13 Based on the comparison, genetic regions from range D3S1250 to D3S18 were suggested as involved with cardiac development (Table 2).13,14,16 Isolating the G6, VHL, and PMCA2 (ATP2B2) genes, they contemplate only the latter as a candidate for septal defects.13 The gene discussed is ATP2B2; the disease is atrial septal defect.