Causes and mechanisms of the registered incidence increase of pediatric thyroid cancer (TC) after the Chernobyl accident, unrelated to the ionizing radiation, were recently reviewed among other topics by Prof. Z. Jaworowski (2010). The main body of evidence (Cardis et al. 2005;Tronko et al. 2006;Davis et al. 2004) in favor of the cause-effect relationship between ionizing radiation and TC among children and adolescents after the Chernobyl accident is based upon the epidemiologic studies (Ron 2009). In the case-control study (Cardis et al. 2005) a retrospective estimation of doses was performed by questioning. The study by Davis et al. (2004) was similar in design. The 'Chernobyl victim syndrome' (Bay and Oughton 2005) was a widespread phenomenon: many patients strived for higher dose estimations to support their status as Chernobyl victims, and provided biased information. Cancer patients could have remembered circumstances related to the exposure better than the controls. Iodine supplementation months after the exposure was reported to reduce the cancer risk threefold (Cardis et al. 2005), although radioiodine would have already been absorbed and there would be no blockage in uptake that could have reduced thyroid dose (Boice 2005). Some aspects of the study design by Cardis et al. (2005), favoring an LNT-type dose-response relationship, were criticized by Scott (2006). The dose-response relationship in the recent epidemiologic study by Zablotska et al. (2011) is even stronger at the low dose level: it can be seen in the graph 2 in this paper that the dose-effect curve (P<0.001) is most steep in the area of minimal doses, then at higher doses it becomes more gently sloping, and the relationship disappears completely at the individual dose level of approximately 3 Sv. A dose-effect relationship of a similar form was reported also previously; but decrease or leveling of TC risk was observed at higher doses, e.g. > 10 Gy of external radiation (Ron et al. 1995). The decrease of risk at higher doses is explained by the effect of cell killing (UNSCEAR 2006;Boice 2005). However, no leveling of TC risk was found by Shore et al.