The mutant phenotypes and lethality may be fully rescued by an UAS sds22 transgene and a genomic rescue build, indicating that sds22 is the gene responsible for the observed phenotypes. sds22 homozygotes die at or before the first larva instar. To check whether loss of sds22 promotes cyst growth and metastasis of RasV12 expressing cells, we expressed RasV12 in sds22 mutant cells using the eyFLP/MARCM BIX01294 system, in which 30% of the attention is typically consists of mutant tissue. In line with previous reports, RasV12 overexpression alone causes benign overgrowth but cells never invade in to the nearby ventral nerve cord or other tissues. Such animals can increase as larvae for up to 15 days after egg-laying and die before pupation or as early pupae, when RasV12 overexpression is combined with homozygous loss of sds22. In contrast, animals indicating RasV12 alone can only grow as larvae for approximately 9 times AEL and then die as early pupae. At 1 week AEL, we observe comprehensive hyperproliferation in eye discs of RasV12sds22 / animals but GFP positive cells are seen in the VNC at only low-frequency. At 15 times AEL we find significant variety of ectopic Meristem GFP positive cells spreading from a primary tumor within the head into the VNC. Furthermore, as RasV12sds22 / tumors grow, the 2 eye antennal disks appear to blend in to one large mass. Together, these results suggest that lack of sds22 can cooperate with RasV12 to promote invasive behavior and tumor growth in a time dependent fashion. Next, we asked if the mutation alone is sufficient to cause tumor growth or metastasis. Just like cells mutant for the neoplastic tumefaction suppressor genes scrib, dlg or lgl, we discover that sds22 mutant clones tend to be more painful and sensitive to cell competition, show Lapatinib molecular weight cell apoptosis, and don’t over proliferate or metastasize. The position of Ras signaling in promoting cell survival has been well-documented. To test whether the effect between lack of sds22 and Ras overexpression is linked to cell survival, we coexpressed the baculovirus caspase inhibitor p35 in sds22 mutant cells utilizing the eyFLP/MARCM system to block cell death. Interestingly, these undead cells stimulate both cell autonomous and non cell autonomous cellular growth and result in a greatly overgrown and folded eye disc and increased tumor like person eyes, indicating that loss in sds22 confers tumor growth when cell death is inhibited. Overexpression of p35 alone doesn’t cause any apparent development disorders. But, we do not find GFP labeled cells outside of the eye antennal disc/optic lobe region, suggesting that blocking cell death is not sufficient to market metastasis of sds22 / cells. Combined with the over-growth phenotype in cooperation with oncogenic Ras, these effects suggest that sds22 mutant cells induce uncontrolled proliferation when combined with an additional genetic change or hit that promotes cell survival. Given that tumor suppressor mutations often require a second hit to express their whole phenotypes, these data suggest that sds22 is a new Drosophila tumor suppressor gene.