Overall survival mechanism used by the Apicomplexan parasites in different host cells. Toxoplasma and Cryptosporidium bind to the surface receptor of host cells through the ligands such as EGF, TNF-α, and parasitic surface proteins such as circumsporozoite protein (CSP). After invasion into the host cells such as enterocytes, macrophages, hepatocytes, etc., the parasite modify the host signaling pathway such as TRADD, NF-kB, PKB/AKT resulting in production and upregulation of anti-apoptotic proteins such as Bcl-2, Bcl-xl, and anti-inflammatory cytokines such as IL-10 thereby stopping cytochrome-c (Cyt-c), TNF-alpha-related-apoptosis-inducing ligand (TRAIL) and BAD, BAX production, and ensuring its survival in the host. Plasmodium parasite mainly modifies host PKB/AKT signaling pathway causing upregulation of anti-apoptotic protein and downregulation of pro-apoptotic proteins such as BAD/BAX. Theileria schizont proliferates uncontrollably within the host macrophages and lymphocytes. Right after invasion, it upregulates anti-apoptotic proteins such as c-FLIP, IAPs, Bcl-2, Bcl-XL, and proto-oncogenic proteins such as C-myc, antiapoptotic genes such as C-FLIP, Bcl-2, and matrix metallo-protein (MMP9) by majorly targeting host signaling pathways such as NF-κB, JNK/AKT, JAK/STAT, phosphoinositide 3-kinase (PI3-K)/MAPK, and TGF-β2. The regulation of these host signaling pathways causes continuous survival and proliferations of the parasite infected cells which are also common in some cases. Chakraborty S, Roy S, Mistry HU, Murthy S, George N, Bhandari V, Sharma P. Potential Sabotage of Host Cell Physiology by Apicomplexan Parasites for Their Survival Benefits. Front Immunol. 2017 8:1261.