In this scenario, the winning player can announce that a checkmate will happen within a given number of moves, assuming a perfect defense by the losing player, or fewer moves if the defending player chooses sub-optimal moves as the game progresses into its inevitable, predicted conclusion. By this analogy, it is suggested, the experience of free will emerges from the interaction of finite rules and deterministic parameters that generate nearly infinite and practically unpredictable behavioural responses. In theory, if all these events could be accounted for, and there were a known way to evaluate these events, the seemingly unpredictable behaviour would become predictable. Another hands-on example of generative processes is John Horton Conways playable Game of Life. Nassim Taleb is wary of such models, and coined the term "ludic fallacy." Compatibility with the existence of science
Certain philosophers of science argue that, while causal determinism (in which everything including the brain/mind is subject to the laws of causality) is compatible with minds capable of science, fatalism and predestination is not. These philosophers make the distinction that causal determinism means that each step is determined by the step before and therefore allows sensory input from observational data to determine what conclusions the brain reaches, while fatalism in which the steps between do not connect an initial cause to the results would make it impossible for observational data to correct false hypotheses.
Not rarely do both contribute to disease in the same individual.In those with FSHD2, although they have do not have a 4qA allele with D4Z4 repeat number less than 11, they still often have one less than 17 (relatively short compared to the general population), suggesting that a large number of D4Z4 repeats can prevent the effects of an SMCHD1 mutation. Further studies need to be done to determine the upper limit of D4Z4 repeats in which FSHD2 can occur.In those with a 4qA allele and 10 or fewer repeats, an additional SMCHD1 mutation has shown to worsen disease, classifying them as both FSHD1 and FSHD2. In these FSHD1/FSHD2 individuals, the methylation pattern of the D4Z4 repeat array resembles that seen in FSHD2. This combined FSHD1/FSHD2 presentation is most common in those with 9 - 10 repeats, and is seldom found in those with 8 or less repeats. The relative abundance of SMCHD1 mutations in the 9 - 10 repeat group is likely because a sizable portion of the general population has 9 - 10 repeats with no disease, yet with the additive effect of an SMCHD1 mutation, symptoms develop and a diagnosis is made.