6-Methylene-4-pregnene-3,20-dione, a potent irreversible inhibitor of rat prostate 5α-reductase in vitro, markedly inhibited the growth of the ventral prostate and seminal vesicles in immature rats when administered s.c. in a daily dose of 100 mg/kg body weight for 35 days. Kidney and testes weights were reduced, together with some reduction in body weight. In the mature rat treated with this steroid in a dose of 40 mg/kg body weight per day for 11 days, marked regression in ventral prostate and seminal vesicles was observed.

Active Rac1 are so imp for improving cytoskeletal systems and necessary for activating IFN-beta & Plcγ2 (which are necessary for regulating TXA2 Synthesis), and are playing imp role for activating CMs and endothelial cells through Ang1 synthesis (mediated by Gp GTP subunits synthesis) then followed by tyrosine kinases function (contain TAT and TAC codons) for Ang2-AT2 productions for adjusting heart contractions and preventing collagen, glycoproteins, and cholesterol accumulations. Angiotensin II type 2 receptors (AT2 receptors) play a modulatory role in blood pressure regulation but produced from Ang1-AT1 by ACE regulated functions , where Tyr codons are playing imp roles in AT1 and AT2 activities and can play so important roles in protecting heart and blood vessels from accumulated cholesterol and glycopeptides and from accumulated glycogen. AT1 receptors promotes the adjustment of various intracellular signaling pathways through Ang2-AT2 production resulting in hypertension, endothelial dysfunction, and recovering the cellular damage.

Rac1 is basis for ATPase, ribosomes repairs, Gactin activities, and regulating fatty Acyl-COA productions (upon OPA1 function) which are main for epidermal growth factor “EGF” synthesis and for both PLCs and IFNs synthesis. Rac1 basically are S6K rich Proline and hydrophobic amino acids that each amino acid especially Proline characterize Rac1 for scpsific functions and activity for regulating specific anti-inflammatory cycles and specific anti-inflammatory growth, that Rac1 has the roles of acting on inflammatory sources for analyzing and producing long fatty chains which will follow the OPA1 oxidative function (which activated by GTPase which promoted by Rac1 active molecules ) for producing fatty Acyl-COAs isoforms which considered as GP-GTP isoforms Gp-GTP gamma, GP-GTP beta, and GP-GTP alpha isoforms where some said that GTPase has been analyzed to give Gp isoforms but GTPase has activated OPA1 enzymes which produced Gp-GTP nuclear isoforms upon effect on long fatty chains, that GP-GTP beta and alpha have the roles of promoting PLCs and IFNs isoforms for anti-inflammatory processes and for anti-inflammatory growth . That The Rho family Rac1-GTPase (Gp isoforms) mediates a variety of signal transduction processes leading to activation of NADPH oxidase, actin cytoskeleton reorganization and anti-inflammatory growth.

Dendritic cells (DCs) play an important role in improving and adapting immune responses, and development of chronic inflammation through producing Interleukin-2 which stimulate beta oxidation processes by OPA1 synthase for promoting both IFN-beta and GC-beta production followed by alpha oxidations for TLR4 and SIRPα1 production and for nucleocytosolic acetyl-CoA alpha production which considered as signature of a “growth specifically for anti-inflammatory growth. Glucocorticoids and glutamine are the basic tools for increasing immune efficiency (regulated by OPA1 enzymes) and the main for regulating the adopted Interferons, that the deficiency in glucocorticoids synthesis and glutamine will suppress immune activities and will lead to deficiency in Interferons productions followed by decreasing in macrophages and T-cells functions. The formation of Glucocorticoid-gamma and IFN-gamma started by the effects of Cox2 on inflammatory sources followed by cytokine kinases production for IL2 synthesis upon synthetase functions followed by synthase for glucocorticoid-beta and IFN-beta productions which followed by phospholipase effect for producing PD-L1 synthesis which promote the progression of ovarian cancer.

The roles of S6K1 is regulating ATPase, and GTPase synthesis, and consequently the endocytic proliferations including endocytic soluble MHC class II synthesis which regulate both SIRPα1 and TLR4 synthesis , where diabetes reflect deficiency in Ser amino acids that reflect deficiency in pyrimidines synthesis consequently deficiency in Estrogen and reflect increasing in androgen synthesis with increasing in consuming in purines (A&G) that lead to decreasing in anabolic processes which depends on presence of adenosine and guanosine stored in ribosimes.