We study the obligate biotrophic oomycete pathogen Albugo candida that causes white rust disease in Brassicaceae. A. candida comprises many races that infect distinct host species. Some A. candida races can also infect various Arabidopsis accessions, thus facilitating the characterization of effectors and resistance genes that are involved in this obligate patho-system. A. candida induces a potent immuno-compromised state in the colonized host plants, which can enable different pathogens to grow and reproduce in the same tissue. Co-habitation of different races on the same host is therefore possible, and could be an important means of generating novel races through the exchange of effector repertoires. Our analyses of multiple A. candida genomes reveal the presence of a novel class of secreted CxxCxxxxxG (abbreviated as CCG) effector family. Every A. candida race has around ~100 CCG secreted proteins which also shows presence/ absence polymorphism. To understand if any of the CCG secreted proteins are recognized by the Arabidopsis TIR-NB-LRR (TNL) class, we screened White Rust Resistance 4 (WRR4) locus that has two paralogs (WRR4A and WRR4B), which confer broad spectrum resistance to various A. candida races. A high-throughput screening with CCG effectors and these two paralogs leads to the identification of multiple non-overlapping CCG effectors that are recognized by these R proteins. Some of these candidate CCG proteins also confer an enhanced susceptibility to other oomycete pathogens in stable transgenic A. thaliana lines. Current experiments aim to functionally characterize these CCG effectors especially for their potential involvement in A. candida mediated immune suppression. I will present an overview of the recent progress of our work on A. candida CCG effectorome and the role of CCG effectors.