Given the tumor suppressor nature of ARMC5, the detection of a second pathogenic event altering ARMC5 at the somatic tumoral level (such as truncating variants or loss-of-heterozygosity), leading to a bi-allelic impairment of the gene, strongly supports the hypothesis of the deleterious effect of the missense variant identified in leukocyte DNA. This evidence concerns the gene ARMC5 and neoplasm.