In addition to these LoF mutations at candidate CVID genes and interacting proteins, we propose other possible monogenic cases produced by missense variants at CVID candidate genes following a dominant (PRKCD, CLEC16A, DOCK8) or recessive models (CR2, PLCG2), as well as in other genes not previously associated with CVID (KMT2C). This evidence concerns the gene PRKCD and common variable immunodeficiency.