We have used a camel cell line model (Dubca) to investigate the effect of heat stress on cell survival. The mechanism(s) of such survival response are very important not only for normal physiological function, but also, in pathological conditions, such as cancer. Those cells that have escaped the normal response to heat are an important model in helping us better understand the intricate signaling change(s) that might have occurred in changing a cell's phenotype from normal to cancerous. Our findings in this study indicate that unlike comparative fibroblast cells (L929), Dubca cells are quite resistant and survive the 42°C heat stress in a time-dependent manner; indeed, the cells even show growth on par with those cells that are kept at the control temperature of 37°C. Expression levels of Akt, an important prosurvival kinase, are uniform, and irrespective of the experimental or control temperature, show basal control levels. In other words, there is no loss of Akt protein level following heat stress at 42°C. Similarly, no significant change in HSP70 expression level is observed. In contrast, the stress transcription factor c-Jun, and the stress activated kinase (Jnk) were induced during this heat-shock condition. This is in line with the fact that suppression of stress kinase Jnk renders cells thermoresistant. On the other hand, acquired tolerance to severe heat shock is associated with downregulation of Jnk.