Replication stress-indepedent synthetic lethality can be triggered in BRCA2-deficient cells by exploiting M phase defects.

Embryonic lethality associated with deficiency of UBIAD1, which synthesizes a vitamin K₂ subtype, results from aberrant ER-associated degradation of the cholesterol biosynthetic enzyme HMG CoA reductase.

STAG1 has been identified as a hardwired genetic dependency of cancer cells harbouring mutations in the cohesin subunit and emerging major tumor suppressor STAG2 holds the promise for the development of selective therapeutics.

Evidence that the small GUY1 protein is a strong candidate for being a male-determining factor is provided via the establishment of Guy1 transgenic lines of mosquitoes that confer complete and stable female lethality.

Mouse genetic manipulations reveal that Cables2 is involved in the progress of gastrulation by interacting with Wnt/β-catenin and the p53 pathways in diminished Rps21 expression.

Co-mutation of two powerful oncogenes in certain cell types may have a lethal effect that explains the mutual exclusivity of the mutations.

ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, and its homolog ARID1B function to maintain chromatin accessibility and active histone modifications at enhancers.

For the first time, the spectrum of genes and pathways interacting with alternative DNA structures called G-quadruplexes in humans is revealed highlighting new possibilities for the pursuit of cancer therapies.

Mice doubly deficient for Naa10 and Naa12 display embryonic lethality, with both enzymes compensating for each other with amino-terminal acetylation of proteins in mouse development.

Increasing the internal pH of cells can induce dysplasia and enhance oncogene-increased cell growth, while decreasing the internal pH combined with oncogene expression leads to synthetic lethality.