cell homeostasis were performed with concentrations of oxysterol (3x10 -5 -10 -4 M) faraway from the physiological and/or pathological one (0.2 and 2x10 -7 M). In our study, we asked the effects of oxysterols (7K and 5'6S) on hepatoma cell lines homeostasis. To this purpose we used concentrations similar to those described in physiological or pathological conditions. Sub-physiological (10 -9 M) to pathological (10 -7 M) oxysterol (7K and 5'6S) concentrations were used to stimulate HepG2 cells. A surprising pro-proliferative effect of 5'6S at sub-physiological (10 -9 M) concentration was observed. This behaviour was confirmed by the synergic increase of ERK1/2 levels. FACS analysis revealed an early progression of cells in S phase at the lowest concentration of 5'6S, while all the remaining concentrations of the two studied oxysterols induced a weakly accumulation of cells in G2/M phase. Apoptosis was absent at all concentration used, except for the highest one (10 -5 M). At this point we asked if cells didn't undergo apoptosis but acquired a senescent profile. Effectively, both 7K and 5'6S, at all concentration used (except for 10 -9 M), induced cell senescence (revealed by SA-ß-gal staining and SIRT1 and p21 over-expression). In conclusion the two oxysterols analyzed have different and in same case opposite effects on hepatocellular line. The main effect is surely the senescence induction, but it is important to highlight the proproliferative effects of 5'6 secosterol at low concentration. Mortalin, a member of HSP70 family protein, has been shown to play an important role in hepatocellular carcinoma (HCC). It has been reported that mortalin is binding to the C-terminal of p53, which acts as a safety guard and is a commonly mutated gene in HCC. In this study mortalin was silenced by specific shRNA in PLC/PRF/5, a HCC cell line constitutively expressing p53ser249, and normal liver cells MIHA, and we found that suppression of mortalin can selectively trigger the mitochondria mediated apoptosis pathway by p53 dependent way in PLC cells. Tunel staining positive cells were only found in the PLC cells mortalin knockdown group, and apoptosis associated protein, such as p53, Bax, Bcl-xl, cleaved-caspase 3, have been screened by western blot after transfection. Quantitative-PCR data also showed that p53 mRNA level are upregulated about 2 folds in mortalin knockdown group compared with the control groups in liver tumor cells. Two p53 inhibitors, PFT-and PFT-, which can reverse this apoptosis was applied to demonstrate p53 dependent way. In summary, knockdown mortalin can selectively kill liver cancer cells through reactive apoptosis by sensitizing mutant p53 in PLC cells, but had no effect on normal cells. The clinical application of this study suggested that motalin specific shRNA might be a potential anti-cancer drug for HCC. Background: NAFLD can proceed to NASH and are at risk of cirrhosis and HCC. Aim was to study profile of Bangladeshi NAFLD patients. Methods: 52 patients with NAFLD were included. Of them 59.6% were males and 40.4% females. Patients were between 12-60 years of age. They presented with dull right upper abdominal ache and/or incidental detection of raised ALT/AST and/or fatty liver on ultrasonography. All tested negative for hepatitis B and C. None had history of alcohol. All underwent per-cutaneous liver biopsy for histopathology. They were also tested for DM, dyslipidaemia, insulin resistance, hypothyroidism and hepatitis C. Their BMI and BP were recorded. Results: 88.5% had NASH. 63.0% of them were males and rest 37.0% females. 11.5% had NAFL. Of them 50% each were males and females.